202 Part 1 Flashcards

1
Q

Where are the instructions that govern cell division

During the first part of the organism’s life, the genes don’t instruct all cells to just divide. They start dividing to do specific things. True or false?

Can human cells be immortal?
What are the only immortal cells that can establish a self perpetuating lineage

A

cell divisions and the instructions governing cell divisions are in the hereditary material(the gene)

4.During the first part of the organism’s life, the genes instruct all cells to just divide. Upon attaining maturity, only specific cells are instructed to continue to divide daily.

5.Human cells can be cultured in the laboratory, but they survive for a few generations and then they die off.

6.The only immortal cells that can establish a self-perpetuating lineage are cancer cells.

HeLa(not Hela) Cells – Brief Overview:

HeLa cells are the first immortal human cells grown in a lab. They were taken from Henrietta Lacks’ cervical cancer tumor in 1951 without her consent.

Key Features:
• Immortal: They keep dividing indefinitely under proper lab conditions.
• Fast-growing: Easy to grow in large amounts.
• Consistent: Useful for repeatable scientific experiments.

How They Were Used:
1. Polio vaccine – Tested virus behavior and vaccine safety.
2. Cancer research – Helped understand cancer cell growth.
3. HIV/AIDS research – Used to study virus infection in cells.
4. Gene mapping & cloning – Helped map the human genome.
5. Drug testing – Tested safety and effects of new drugs.
6. COVID-19 vaccines – Used in early research and development.

HeLa cells have contributed to thousands of studies, but their use raised ethical questions about consent, privacy, and compensation.

Here are more key features of HeLa cells:
1. Immortality – They divide endlessly, unlike normal human cells that stop after a few divisions (called the Hayflick limit: The Hayflick Limit is the number of times a normal human cell can divide before it stops)
2. Rapid Growth – HeLa cells double in number about every 20–24 hours.
3. Durability – They can survive in harsh lab conditions and even cross-contaminate other cell cultures.
4. Versatility – Can be infected with viruses, exposed to radiation, or used to test chemicals and still grow — making them ideal for research.
5. Easy to transport – They stay alive longer during shipping than most cells.
6. Human origin – Even though they act differently from normal cells, they are human cells, so results are more relevant to human biology.
7. Cancerous – They are cancer cells, so they grow abnormally and don’t follow normal cell rules — useful for studying how cancer behaves.

Let me know if you want this turned into a quick table or flashcard format for easier study.

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2
Q

Explain 4 reasons why cells divide after birth

State four ways cells know when to divide

A

Cells divide because very few cells last an individual’s lifetime and therefore need to be replaced when they become too old to function well or when they die off.

2.Once the cell attains a certain size, the speed of diffusion to supply the necessary nutrients reduces making cells less efficient.

3.An individual develops from childhood to adult. New cells to needed to maintain this development, hence cells need to divide to create more cells for growth and development

4.The need for continual existence and therefore the need to produce sex cells for reproduction (fertilization).

5.In (4) above, the need to ensure normalcy in reproduction ensures haploid production of sex cells

How do cells know when to divide
1. When neighbouring cells die opening up space in the tissue, the space needs to be occupied by new cells.
2. When they are stimulated by growth factors, which are chemical signals secreted by blood platelets, kidney cells and other sources, cells divide in response.
3. When diffusion alone cannot ensure adequate exchange of materials between cells and environment because they’ve grown bigger
4. When they grow large enough and are capable of producing enough cytoplasmic material to distribute to two daughter cells.
5. When they have everything in place to ensure successful replication of their DNA successfully so they can give each daughter cell a duplicate set of genes.

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3
Q

Why do cells divided generally at first and then divide more specifically later on

A

Great question!

Simple Answer:

In early development, cells divide generally to make more cells fast. Cells divide generally just to make more cells quickly.
Later, they divide specifically to become special cell types (like muscle, nerve, or skin cells).

Why This Happens:
1. Early Stage (General Division):
• The body needs to grow quickly from a single cell (zygote) into a ball of cells.
• These early cells are unspecialized (stem cells) and can become anything.
2. Later Stage (Specific Division):
• As the body forms, cells receive signals that tell them what to become.
• They start differentiating — becoming specific types based on location and needs.
• Now, they divide in a controlled way to maintain or repair tissues (e.g., skin cells replacing old skin).

Example:
• In the embryo: cells are like clay — can become anything.
• In the adult: cells are like bricks — already shaped for a purpose.

Let me know if you’d like a diagram or short version for easy recall.

Great follow-up!

What kind of signals tell cells what to become?

Cells receive four main types of signals that guide their specialization (differentiation):

  1. Chemical Signals (Molecules)
    • Growth factors, hormones, and cytokines.
    • Example: Nerve growth factor tells a stem cell to become a nerve cell.
  2. Cell-to-Cell Contact
    • Neighboring cells send signals through direct contact.
    • Helps organize tissues and tell a cell what it should become.
  3. Position in the Body (Spatial Signals)
    • A cell’s location in the embryo affects which genes turn on.
    • Example: Cells near the spine may become bone or spinal cord tissue.
  4. Environmental Signals
    • Oxygen levels, nutrients, or even pressure can affect cell behavior.

Summary (Quick Recall):

Signals = Chemicals + Contact + Location + Environment

Let me know if you want examples from real tissues (like skin or blood).

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4
Q

When adulthood is reached, which cells continue to divide daily?
Which tissues stop routinely producing new cells after birth?
Why does this happen?

What’s the evidence that cell division isn’t a random event?

A

Daily: rbcs and skin cells

Nervous tissue stop routinely producing new cells after birth

Is cell division a random event
1. When adulthood is reached, specific cells such as skin and blood cells continue to divide daily.
2. Others such as nervous tissue after birth no longer routinely produce new cells.
3. Liver cells has a remarkable ability to regenerate and can do so from a third of the original cell within a short time.
4. Some cells can also move to a state where growth can be halted for a period before exiting that state and initiating cell division
This tells us that cell division is not just a random event but a well controlled and coordinated event.

Some cells can halt growth temporarily before dividing – what does this mean?

This refers to a phase called G₀ phase (G-zero) in the cell cycle.
• Normally, cells go through stages to grow and divide (G1 → S → G2 → M).
• But some cells pause in G₀, which is like a resting state.
• In G₀, the cell doesn’t divide but can stay alive and do its normal work.
• Later, some cells can exit G₀ and re-enter the cycle to divide again if needed (e.g., liver cells during injury).

Why is this useful?
It allows the body to control when and where cells divide, avoiding too much or unnecessary cell growth.

Why don’t nervous tissues routinely produce new cells after birth?

Most nerve cells (neurons) exit the cell cycle permanently and stay in G₀ forever after birth.

Why?
• Nerve cells are highly specialized and don’t regenerate easily.
• Dividing might disrupt the brain’s connections and memory.
• The nervous system values stability and function over regeneration.

However, a small number of stem cells in certain brain areas (like the hippocampus) can still produce new neurons, but this is limited.

After Birth:
• After birth, synaptogenesis continues at a rapid pace, especially during the first few years of life. The brain is highly plastic, meaning it’s very adaptable and continues to form new connections and strengthen existing ones based on experiences and learning.
• However, once neurons mature and the brain reaches certain stages of development, the rate of neurogenesis and synaptogenesis slows down.

In summary, neurons do form connections before birth, and these early connections are crucial for brain development and the proper functioning of the nervous system as the baby grows. After birth, this process continues, but at a slower pace.

Great follow-up!

Here’s a simple explanation:

Why dividing would disrupt the brain’s connections:
1. Neurons are highly connected
• Each neuron forms thousands of connections (synapses) with other neurons.
• These connections help with memory, learning, movement, and more. The nerve cells move into the Gzero stage sometime after birth. So the nerve cells form connections which contain memories. If the cells divide, it can lead to breakage of those connections and loss of memories.

G0 is a particular phase within the cell cycle where a cell is not dividing, while quiescence is a general term for cells that are inactive but can potentially resume division when needed.

2.	Division would break those connections
•	For a cell to divide, it has to stop working, copy its DNA, and split into two new cells.
•	A dividing neuron would have to disconnect from its network, losing the signals and memories it stores.
3.	Risk of mistakes
•	The brain’s wiring is very precise. If neurons started dividing, there’s a risk of errors, like:
•	Wrong connections
•	Signal confusion
•	Potential for diseases (like brain tumors)

So in summary:
Neurons don’t divide because it would disconnect important brain networks and risk damaging how the brain works. Stability is more important than regrowth in this case.

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5
Q
  1. If cell division is not random,
    → Then there must be a control system regulating how and when cells divide.
    1. This control system must monitor both internal and external conditions,
      → To ensure the cell only divides under the right circumstances (e.g., enough nutrients, no DNA damage, space available, etc.).
    2. The system must be receptive and responsive to signals,
      → So it can react appropriately to environmental cues or signals from other cells (e.g., growth factors, stress signals).
    3. This control system has been identified as specific regulatory enzymes,
      → Mainly cyclins and cyclin-dependent kinases (CDKs), which work together to control progression through the cell cycle.

This is the foundation of how cell cycle regulation prevents uncontrolled division, like what happens in cancer when this system fails.

A
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6
Q

The cell must duplicate the dna in the chromosomes properly and then segregate those copies into two daughters cells
Why isn’t interphase entirely a resting stage as believed or assumed at first?

A

The process of cell division was believed to be a series of events that must take place in a coordinated manner thus the cell cycle concept was proposed.
4. The cell cycle is defined as the life of a cell from the first time it is formed from a parent until its own division into two cells.
5. Cell division was also found not to be occurring all the time and that in between divisions, there was a resting phase where no visible activity was assumed to take place. This phase was given the name interphase.
6. Then, it was discovered that DNA replication occurs during interphase, and the interphase was after all not a resting phase.

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7
Q

Originally the cell cycle was divided into two phases and later into four stages. Name the two phases and the four stages

State what happens in each of the four stages of the cell cycle
Which phase is the shortest
Which is the longest

A

The shortest phase of the cell cycle is the Mitotic phase (M phase) and the longest phase of the cell cycle is G-1 phase(maybe I’ll stick with interphase)
So in conclusion, G1 deals with the cell becoming bigger in size and components of the cell duplicating. It also prepares the chromosomes for duplication or replication
S deals with duplication of the chromosomes and proteins for DNa are synthesized too
G2 makes sure the cell has been replicated properly and is ready to enter the M phase and it duplicates the centrioles and produces enzymes that control cell division.

All remaining proteins needed for cell division are synthesized now that the cells prepares to divide including synthesizing tubulin for construction of the microtubules of the spindle apparatus.

The cell cycle concept
1. The cell cycle proposed either a two-phase or 4 stage cycle and the latter is more acceptable.

Two phase is just interphase(non dividing phase)
Mitosis phase or M phase (dividing phase)
But now we know that interphase isn’t entirely a resting phase and other things go on there so the four stage was brought up.

So now interphase has G1, S, G2 and the final stage is M

The “G” in G1 and G2 originally stood for “Gap”, because scientists first thought these were simply “gaps” between DNA replication and cell division.
However, we now know that active growth and preparation happen during these phases, so it’s also correct to describe them as “Growth phases.”

During the G1 the cell increases in mass and doubles the number of cytoplasmic components and accumulate all materials needed to replicate
DNA. Chromosomes are not duplicated here.

Then there is the S-stage (synthesis) of the cycle. This is the period of DNA synthesis or replication takes place. The proteins associated with DNA are also synthesized during this stage. So chromosomes are duplicated here

During G2, various metabolic events including replication of centrioles and synthesis of enzymes that control cell division occur. It makes sure the cell is ready for division and checks if there were errors with replication of the DNA. Cell prepares to divide

G1 checkpoint (before S phase) checks if cell DNA is ready to replicate(If failed: The cell may enter a resting state (G0) or undergo apoptosis (programmed cell death).)
G2 checkpoint (before M phase) checks if cell is ready to divide and if replication was done correctly

There is the M-stage (mitosis) which is the main division stage and it includes both mitosis and cytokinesis

S phase = Initiation of centrosome duplication.
• G2 phase = Completion of centrosome duplication.

S phase takes longer to do than all the phases.(I’m seeing something else)

Phases of the cell cycle
The cell cycle starts with the interphase which has three stages defined as the
G1, S and G2 phases. Next is the real process of cell division - prophase, metaphase, anaphase and telophase.
The length of the cell cycle varies from one cell type to the other. Stomach and skin cells divide rapidly, bone and cartilage cells divide slowly and nerve cells not at all.
After division, some cells leave the cycle for a rest in the G,, and others cease to divide for days, years or forever. Such cells are said to be in the Go phase.
The balance between actively dividing cells and those in the Go phase is important in determining the number of cells in the body.

G, (first growth) phases (6-9 hours)
This phase is very active because the cells grow in size and cellular organelles and proteins are doubled. Late in G1, the cells prepare to duplicate their chromosome.

Checkpoint 1
• The first checkpoint of cell division occurs is at the G1 stage.
• All the conditions needed for DNA replication must be met. Thus, a control system must respond to information received from the processes that it controls.
• At this stage the sensors must detect the complete synthesis (doubling) of the cellular components.
• If these conditions are not met the system is forced back to the Go stage for the process to stop entirely or the needed corrections are made before being allowed to proceed.
• This is to prevent disaster if the cycle proceeds prematurely to the next stage.
• Checkpoints can also be regulated by extracellular signals from other cells for promotion or inhibition of proliferation.

S (synthesis) phase (6 - 8 hours)
The synthesis of histones and other proteins associated with DNA is markedly increased. DNA replicates doubling the chromosomes so each of the chromosomes becomes a complex of two identical sister chromatids.

G2 phase (2-4 hours)
All remaining proteins needed for cell division are synthesized now that the cells prepares to divide including synthesizing tubulin for construction of the microtubules of the spindle apparatus.
The second checkpoint is here. A number of proteins scrutinize the cell’s DNA, making sure it is structurally intact and properly replicated. The cell may pause at this point to allow time for DNA repair, if necessary.

Mitosis(hour or two.)
Mitotic cell division now occurs. This is the shortest phase an only about an hour or two

Points to note:
> Some cells such as liver cells divide less frequently. These cells can spend months in interphase before going through a brief mitotic phase.
> Other cells such as hair follicles and skin cells cycle very frequently.
• Some cells such as red blood cells divide a number of times, then lose their nuclei and leave the cell cycle never to divide again.
• After mitosis, some cells re-enter G1, to go through the cell cycle phases again, others enter and wait, and others enter never to divide or enter an extended phase called Go.
• For the Go cells, an appropriate signal stimulates them to re-enter the cycle and divide.

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8
Q

Why do skin cells and gut cells divide continuously?
Where will you put an arrested nerve cell in the cell cycle for it to finish it?
What about an arrested cardiac cell
What’s the function of kinases and cyclins in the cell cycle?
How do cells control cell division?

A

Ah, got it — you meant skin and gut, not “hit and skin.” Thanks for the clarification!

Why do skin and gut cells divide continually?

Because both are high-turnover tissues exposed to constant damage, friction, or chemical stress, so they need to renew themselves rapidly to maintain function and protection.

  1. Skin
    • It acts as a barrier against the environment.
    • Cells in the outer layer (epidermis) constantly die and shed, so new ones must replace them.
    • Stem cells at the base of the skin keep dividing to replenish lost cells.
  2. Gut (intestinal lining)
    • The gut lining faces digestive acids, enzymes, and food movement, which can damage cells.
    • Cells in the lining are replaced every few days.
    • Stem cells in the intestinal crypts divide rapidly to keep the lining intact and functioning.

In short:
Skin and gut cells divide continually because they are exposed to constant damage and need fast, regular renewal to stay healthy.

Let me know if you want a simple diagram or memory tip for this!

Regulation of the cell cycle
1. Some cells such as skin cells divide continuously throughout the life of the organism, whilst other arrest at certain stages of the cycle.
2. For example, if the nucleus of an arrested nerve cell is placed in the cytoplasm of an S-stage cell, it finishes the cell cycle. It is thus obvious that nerve cells are arrested in the G1 stage. There must therefore be a checkpoint at this stage.
3. Likewise, if an arrested cardiac cell is fused with a cell in the M-stage, it finishes the cell cycle. Therefore, cardiac muscle cells must be arrested in the G2 phase. Again, there must be another checkpoint at this stage.
4. There must thus be both repressive and stimulatory sensors that causes the cell to proceed through these two checkpoints.
5. Two types of proteins - kinases and cyclins have been identified as playing major roles in G, to S and G, to M stages.
6. A kinase removes a phosphate group from ATP and adds it to a protein.

You’re thinking deeply — I love that! Let’s break both parts down clearly:

  1. What are the “sensors” that regulate the checkpoints?

The sensors are mainly proteins and protein complexes that monitor conditions in the cell and decide whether to allow or block progression through the cell cycle.

These include:

a. Stimulatory sensors (promote progression):
• Cyclins – Regulatory proteins that increase and decrease at different cell cycle stages.
• CDKs (Cyclin-Dependent Kinases) – Enzymes that become active when bound to cyclins; they phosphorylate target proteins to move the cycle forward.

b. Repressive sensors (block progression if there’s a problem):
• p53 – A tumor suppressor that halts the cycle if there’s DNA damage, especially at the G1 checkpoint.
• p21 – Activated by p53, it inhibits CDKs, blocking progression.
• ATM/ATR proteins – Detect DNA damage and activate repair pathways or stop the cycle.
• Chk1/Chk2 – Kinases that stop the cycle by inhibiting CDC25, a phosphatase needed for CDK activation.

So in short:
• Sensors = Cyclins/CDKs (stimulatory) and p53, ATM, ATR, Chk1/2 (repressive)

  1. What will a cyclin do?

Let’s clear this up:

Kinase:
• A kinase (like CDK) adds a phosphate group from ATP to a target protein — this often activates or inactivates that protein.

Cyclin:
• A cyclin does NOT phosphorylate anything on its own.
• Instead, a cyclin binds to a CDK (cyclin-dependent kinase) and activates it.

So:

A cyclin’s job is to bind and activate a CDK. The cyclin-CDK complex then adds phosphate groups to specific proteins to push the cell through a checkpoint.

Summary:
• Sensors = Cyclins/CDKs (stimulatory), p53, p21, ATM/ATR (repressive)
• Cyclin itself doesn’t phosphorylate — it activates CDKs, which do the phosphorylation.

Let me know if you want a chart or analogy to remember this better!

Exactly — you’ve got the idea! Let’s make it super clear:

  1. Phosphorylation (by CDK-cyclin complexes) = “Go” signal
    • When a cyclin binds to its CDK, it forms an active cyclin-CDK complex.
    • This complex phosphorylates specific proteins.
    • Those phosphorylated proteins activate processes like:
    • DNA replication (in S phase),
    • Spindle formation (in M phase),
    • Chromosome separation, etc.
    • So, phosphorylation = activating the next step in the cycle.
  2. Removal or breakdown of the cyclin = “Stop” signal
    • Cyclins are not permanent — they are destroyed at the right time.
    • When the cyclin is degraded, the CDK becomes inactive.
    • This stops the activity that was pushing the cell forward.

Example:

In S phase:
• Cyclin A + CDK2 → phosphorylates replication proteins → DNA replication begins.
• Later, Cyclin A is degraded → CDK2 turns off → replication ends.

So yes:
• Phosphorylation = Activation
• Cyclin removal = Inactivation

That’s how the cell cycle is tightly controlled — like a switch that turns on and off at the right times.

Want a quick analogy?

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9
Q

How do cells control division?

A

So, cells control division by
1. The use of check points which monitor and control the progression from one stage to the other.
2. At each check point, specialized proteins ensure that the required conditions have been met before the cell can enter the next phase.
3. Kinases which becomes activated by combining with cyclins at two critical checkpoints in the cycle, phosphorylates an inhibitory protein which in turn triggers the beginning of S and M stages. The inhibitory protein is Rb. The inhibitory protein you’re referring to is called retinoblastoma protein (Rb protein).

Here’s how it works simply:
1. Cyclin-dependent kinases (CDKs) combine with specific cyclins to become active at cell cycle checkpoints.
2. The active cyclin-CDK complex phosphorylates the Rb protein.
3. Unphosphorylated Rb binds to E2F, a transcription factor, and blocks cell cycle progression.
4. Once phosphorylated, Rb releases E2F, allowing the transcription of genes needed for S phase (DNA replication).

Summary:
• Inhibitory protein = Rb protein
• Function = Prevents progression into S phase
• Phosphorylated by = Cyclin-CDK complex
• Result = Entry into S phase (and eventually M phase)
4. Afterwards the cyclins and kinases dislodge, the cyclins are destroyed and the kinase reverts to the inactive state.
5. Typically, a cyclin should combine with a kinase only when growth factors are present. But a cyclin gone awry combines in the absence of growth factors and the result is uncontrollable cell growth as seen in cancers.
6. Tumour suppressors e.g. p53 controls production of proteins/growth factors that can combine with cyclins, rendering them inactive, so that it does not get the chance to bind to a kinase.

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10
Q

So, cells control division by
The use of check points which monitor and control the progression from one stage to the other.
At each check point, specialized proteins ensure that the required conditions have been met before the cell can enter the next phase.
what are the specialized proteins?

A

Perfect setup! Let’s now name the specialized proteins that regulate the checkpoints and control cell division:

Specialized Proteins Involved in Cell Cycle Checkpoints:

  1. Cyclins
    • Regulate the timing of the cell cycle.
    • Different types (e.g., Cyclin D, E, A, B) are active at different stages.
    • They activate CDKs.
  2. CDKs (Cyclin-Dependent Kinases)
    • Enzymes that phosphorylate target proteins to move the cell into the next phase.
    • Only active when bound to a cyclin.
  3. CDK Inhibitors (CKIs)
    • Examples: p21, p27, p16
    • These block CDK activity to pause the cycle if conditions are not right.
  4. p53
    • A “guardian of the genome.”
    • Detects DNA damage and activates p21 to block the cycle.
    • Can also trigger apoptosis if damage is too severe.
  5. ATM and ATR
    • Sensors for DNA damage.
    • Activate checkpoint kinases when problems are found.
  6. Chk1 and Chk2 (Checkpoint kinases)
    • Activated by ATM/ATR.
    • Prevent progression by inhibiting CDC25, which is needed to activate CDKs.
  7. APC/C (Anaphase-Promoting Complex/Cyclosome)
    • Triggers transition from metaphase to anaphase in mitosis.
    • Helps destroy cyclins to end a phase.

In short:

Cyclins, CDKs, CDK inhibitors, p53, ATM/ATR, Chk1/2, and APC/C are the key specialized proteins that act at checkpoints to control cell division.

Let me know if you want a memory tip or visual to help recall these!

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11
Q

When do cells know to stop dividing?

A

When do cells know to stop dividing
1. Mainly by contact inhibition when they contact neighbouring cells.
2. External cues that initiate cell division now initiates its inhibition
3. Withdrawal or break down of these external cues
4. Lack of nutrients

Of interest:
1. What is amazing during cell division is that enzymes and proteins selectively access, activate and silence information in all DNA.
2. They make base by base copies of all the bases in every DNA molecule all during the G1 phase. So you’re preparing the cell to have all it refs for replication of its DNA in S phase
3. Once S begins, DNA replication proceeds at about the same rate for all cells of a species.
4. The cell cycle lasts about the same time for cells of the same type.

Great thoughts — let’s go through each part and clarify where needed:

When do cells know to stop dividing?

Yes — you’re absolutely right:

1. Mainly by contact inhibition — when cells touch neighboring cells, they receive signals to stop dividing.

Other ways cells know when to stop dividing include:
• DNA damage detection (via p53).
• Loss of growth signals (like growth factors).
• Telomere shortening (in aging cells).
• Hormonal or environmental cues.

Interesting Point 1:

“What is amazing during cell division is that enzymes and proteins selectively access, activate and silence information in all DNA.”

Yes! This refers to epigenetic control:
• Some genes are turned on, others off, depending on the cell’s needs.
• This regulation ensures only the right genes are expressed during each stage.
• It’s done by transcription factors, histone modifiers, and DNA methylation.

Interesting Point 2 (Correction):

“They make base by base copies of all the bases in every DNA molecule all during the G1 phase.”

This needs a correction:
• The actual copying (replication) of DNA happens in the S phase, not G1.

Let’s fix it:

DNA replication (copying all bases) occurs during the S phase of the cell cycle. In G1, the cell just grows and prepares materials needed for DNA replication.

Summary:
• Cells stop dividing due to contact inhibition, signals, or DNA damage.
• DNA is carefully regulated by proteins that turn genes on or off.
• DNA copying happens in S phase, not G1.

Let me know if you want a timeline of G1, S, G2, and M with key events!

Great question! Here’s a simple explanation of how touching neighboring cells (contact inhibition) tells a cell to stop dividing:

What is Contact Inhibition?

Contact inhibition is a process where normal cells stop dividing when they bump into each other or fill up the space.

How does it work?
1. Cells have surface proteins (like cadherins and integrins) that can sense when another cell is nearby or touching them.
2. When cells touch each other, these surface proteins send signals inside the cell that say:
“We’re surrounded — no more space — stop dividing.”
3. These signals turn off the cyclins/CDKs or activate inhibitors (like p27) that block the cell cycle.

What’s the result?
• Cells pause in the G1 phase.
• No DNA replication or division happens.
• The tissue maintains a proper size and shape.

Extra note:
• Cancer cells often lose contact inhibition, so they keep dividing even when crowded, which is one reason tumors form.

Let me know if you want a one-line summary to memorize it!

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12
Q

Difference between sister chromatids and non sister chromatids
What is a homologous pair

A

Sister chromatids is two chromatids from one parent joined by a centromere
Non sister is two chromatids from two different parents joined by a centromere
Homologous pair is one sister chromatid and one non sister chromatid

You’re almost there — you’re thinking in the right direction! Let’s clarify it step by step:

  1. Sister Chromatids:
    • These are two identical copies of one chromosome made during DNA replication.
    • They are joined together at the centromere.
    • Same genes, same alleles (since they’re copies of each other).
    • From the same parent.Example: After DNA replication, the chromosome from your mom becomes two identical sister chromatids.
  2. Non-sister Chromatids:
    • These are chromatids from homologous chromosomes — one from mom, one from dad.
    • They carry the same genes but may have different alleles.
    • They are not joined by a centromere.
    • During meiosis, crossing over happens between non-sister chromatids.
  3. Homologous Pair:
    • A homologous pair consists of two chromosomes:
    One from your mom + one from your dad.
    • Each chromosome in the pair may be duplicated, meaning:
    • One homologous chromosome = 2 sister chromatids
    • So, a homologous pair can include 4 chromatids in total:
    • 2 sister chromatids from mom
    • 2 sister chromatids from dad
    • In meiosis, these 4 chromatids line up together.

In short:

Term What It Is From Same Parent? Joined by Centromere?
Sister Chromatids Identical copies of one chromosome Yes Yes
Non-sister Chromatids From homologous chromosomes (mom + dad) No No
Homologous Pair 1 chromosome from mom + 1 from dad No No (but each has its own centromere)

Let me know if you want a drawing or visual summary to help!

Great question! Here’s a simple breakdown of the difference between a chromatid and a chromosome:

Chromosome:
• A complete DNA molecule with proteins.
• Carries genetic information.
• In humans, we have 46 chromosomes (23 pairs).
• A chromosome can exist as:
• One chromatid (before replication)
• Two chromatids (after replication) — still counted as one chromosome.

Chromatid:
• A single copy or strand of a replicated chromosome.
• After DNA replication, each chromosome has two sister chromatids.
• Sister chromatids are joined at the centromere.
• Once they separate (during cell division), each becomes its own chromosome.

Quick Summary:

Term Before DNA Replication After DNA Replication
Chromosome 1 chromatid 2 sister chromatids = 1 chromosome
Chromatid A single DNA strand One half of a replicated chromosome

Analogy:

Imagine a book:
• 1 book = 1 chromosome
• When you photocopy it (replication), you now have two identical pages bound together — those are sister chromatids, still counted as one book/chromosome until they separate.

Want a one-liner to memorize this?

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13
Q

Where do the centrosomes divide before mitosis begins ?
Function of centrosome
What is mitosis?
Importance of mitosis

A

The centrosome, a microtubule divides in the G, phase before mitosis begins.
They organize the spindle, the structure, that brings about chromosome movement during division.

Mitosis
This division by the somatic or body cells is responsible for the creation of new identical diploid daughter cells from a single diploid cell. It thus includes cytokinesis.

Mitosis serves the following
• Development of an individual’s over 70 trillion cells from fertilization
• Growth of all tissues and organs after birth
• Replacement of cells that die Repair of damaged tissues

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14
Q

Difference between eu and heterochromatin
Which of them condenses in cell division

A

The chromatin that is condensed and can be easily viewed under the microscope is called heterochromatin.

Explanation:
• Heterochromatin is tightly packed and inactive, meaning it’s usually not involved in gene expression.
• It appears as dense, dark-staining regions under a microscope during cell division.

In contrast:
• Euchromatin is less condensed, actively involved in gene expression, and is lighter under a microscope.

Key Points:
• Heterochromatin: Tightly packed, visible under the microscope, inactive.
• Euchromatin: Loosely packed, active, less visible under the microscope.

Let me know if you want more details on this!

Ah, I see! In terms of cell division, the chromatin that condenses and becomes visible under the microscope is euchromatin, not heterochromatin.

Here’s why:
• Euchromatin is the active chromatin that is loosened and uncoiled during interphase. It is where gene expression occurs.
• During cell division, euchromatin condenses into chromosomes, which can then be easily observed under the microscope.

Heterochromatin:
• Heterochromatin is already in a tightly condensed form, so it’s not typically involved in gene expression during interphase. It remains condensed and dark-staining throughout most of the cell cycle, but it doesn’t further condense in preparation for division.

Summary:
• Euchromatin condenses during cell division and becomes visible as chromosomes.
• Heterochromatin is already condensed and generally remains inactive.

Let me know if you need further clarification!

It seems like there might have been a typo in your question. I believe you meant to ask about “heterochromatin” instead of “heywrochromqtin.”

Heterochromatin:

Heterochromatin is a form of highly condensed chromatin that plays several important roles in the cell:

Roles of Heterochromatin:
1. Gene Regulation:
• Heterochromatin is generally gene-inactive (not expressed), which helps silence certain genes. It plays a role in regulating gene activity by keeping specific regions of the genome tightly packed and inaccessible to the transcription machinery.
2. Maintaining Chromosome Structure:
• Heterochromatin helps in maintaining the structural integrity of chromosomes. It is found around the centromeres and telomeres, regions essential for the proper organization and movement of chromosomes during cell division.
3. Genomic Stability:
• By keeping certain regions of DNA tightly packed, heterochromatin helps in protecting the genome from damage and maintaining genomic stability. It can prevent transposable elements from being activated.
4. X-Chromosome Inactivation:
• In females, one of the X chromosomes in each cell is inactivated and remains as heterochromatin. This ensures that the two X chromosomes in females do not result in double the gene dosage, which is necessary for proper development.

Summary:

Heterochromatin is mainly used in gene silencing, maintaining chromosomal structure, and ensuring genomic stability. It helps keep certain regions of the genome inactive and tightly packaged.

Let me know if you’d like more details!

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15
Q

Explain the phases from interphase to mitosis in detail.

A

G2 of Interphase
1. Chromosomes yet
to be condensed
2. Centrosomes duplicates into centrioles
3. Nucleolus still visible
Witterdule
Chromosome, consisting
onwe sater chromatos
Prophase
1. Chromosomes shorten and thicken into compact rods of sister chromatids
2. Mitotic spindle begins to form
3. Nuclear membrane breaks down and nucleolus disappears
Kinetochore|
Kinetochore
microtoule
Prometaphase
1. Nuclear envelope fragments
2. Microtubules from centrosome invade nuclear area
Chromosomes now have a kinetochore

Metaphase
1. Centrosomes at opposite poles
Chromosome line along midline of the cell. metaphase plate
Fibres of aster attach to plasma membrane
Longest stage of mitosis
(20 mins)
Daughter chromosomes
Anaphase
1. An enzyme causes centromeres to divide and sister chromatids of each chromosome pair separate and move to the end of the poles
2. The centromere leads with the arms trailing behind.
3. Sister chromatids are identical and each daughter cell receives one chromatid from each chromosome making the daughter cells genetically identical
Nue earl
forming
Telophase
1. Chromatids cluster on each side of the cell.
2. RER produces a new
nuclear envelope
3. Two new daughter nuclei form in the cell
4. Nucleoli reappear

Interphase (G1, S & G2):
The cell replicates its cytoplasmic components and DNA to get ready for the next cycle. Chromosomes are not clearly discerned in the nucleus.

Prophase:
Chromatin in the nucleus begins to condense and becomes visible in the light microscope as chromosomes. The nucleolus disappears and nuclear envelope fragments. The sister chromatids of a chromosome are attached at the centromere. Centrioles begin moving to opposite ends of the cell and the spindle fibers extend and spindles attach to the centromeres (prometaphase)

Metaphase:
Spindle fibers align the chromosomes along the middle of the cell nucleus. This line is referred to as the metaphase plate. This organization helps to ensure that in the next phase, when the chromosomes are separated, each new nucleus will receive one copy of each chromosome.
Chromosomes are easier to visualize here by light microscope. Thus clinical diagnosis of chromosome disorders is based on metaphase chromosomes

Anaphase:
The two sister chromatids of each duplicated chromosome separate at the centromere and move to opposite sides of the cell. Motion results from a combination of movement along the spindle microtubules and through the physical interaction of polar microtubules.
Anaphase is delayed until all chromosomes are positioned at the metaphase plate.

Telophase:
Chromatids arrive at opposite poles of cell, and new membranes form around the daughter nuclei. The chromosomes are no longer visible under the light microscope. The spindle fibers disperse, and cytokinesis or the partitioning of the cell may also begin during this stage.

Cytokinesis:
In animal cells, cytokinesis results when a fiber ring composed of a protein called actin around the center of the cell contracts pinching the cell into two daughter cells, each with one nucleus.

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16
Q

clinical diagnosis of chromosome disorders is based on the chromosomes in which part of mitosis

Explain

A

Yes, that’s correct! Metaphase chromosomes are the easiest to visualize under a light microscope and are therefore used for clinical diagnosis of chromosome disorders.

Here’s why:

Why Metaphase Chromosomes Are Easier to See:
• During metaphase (a stage of mitosis), the chromatin (DNA) is fully condensed into distinct, thick, and compact structures known as chromosomes.
• These condensed chromosomes are highly visible under a light microscope because they are shortened and thicker compared to their uncondensed form in interphase (when they exist as chromatin).
• Each chromosome consists of two sister chromatids, which are joined at the centromere.

Clinical Diagnosis of Chromosome Disorders:
• Chromosome disorders (such as Down syndrome, Turner syndrome, and Klinefelter syndrome) often involve structural changes to the chromosomes (e.g., extra chromosomes, deletions, or duplications).
• Karyotyping is a technique used to examine metaphase chromosomes. It involves:
1. Collecting cells (e.g., from a blood sample).
2. Inducing the cells to divide until they reach metaphase.
3. Staining and visualizing the chromosomes under a microscope.
4. Arranging the chromosomes into a karyotype, which can reveal:
• Chromosome number (e.g., extra or missing chromosomes).
• Chromosome structure (e.g., translocations, deletions, or duplications).

Summary:
• Metaphase chromosomes are condensed and distinct during metaphase, making them easier to visualize with a light microscope.
• This makes them the ideal stage for identifying and diagnosing chromosome disorders through techniques like karyotyping.

Let me know if you need more details or examples of chromosome disorders!

In the context of visualizing chromosomes under a light microscope during metaphase, the chromatin is condensed and forms chromosomes that can be easily seen. This condensed chromatin primarily consists of euchromatin, although heterochromatin can also be part of the chromosomes.

Key Differences:
1. Euchromatin:
• Active chromatin that is loosely packed during interphase.
• Becomes condensed during cell division (particularly during metaphase) to form visible chromosomes.
• It contains genes that are actively transcribed and expressed.
2. Heterochromatin:
• Tightly packed and inactive chromatin that remains condensed even during interphase.
• Found near the centromere and telomere regions of chromosomes.
• Non-active in terms of gene expression and doesn’t participate in transcription.

During Metaphase:
• Both euchromatin and heterochromatin are part of the chromosomes.
• Euchromatin becomes more tightly condensed and forms the easily visible chromosome structures under the microscope.
• Heterochromatin remains condensed but is generally not involved in gene expression during this time.

Summary:
• Euchromatin is the chromatin that undergoes condensation during cell division to form visible chromosomes during metaphase. While heterochromatin is also part of the chromosome structure, it remains more condensed and inactive.

Let me know if you’d like further clarification!

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17
Q

Cell division is all about efficiency and timing
1. A mechanism for checking completion of stages before progression e.g. entry
S phase can only happen if events in G1 are completed. - check points
2. A mechanism that initiates events in the correct order by turning each event on at a specific time, thus providing a fix amount of time for the completion of each event. - flow of production
3. A mechanism to ensure that each event is triggered only once per cycle - efficiency
4. On/off switches that trigger events in a complete irreversible fashion. It will be disastrous if chromosome condensation or nuclear envelope breaks down but not completed - automation
5. Backup mechanisms to ensure that the cycle can work properly even when parts of the system malfunction
6. Adaptability so that the systems behaviour can be modified to suit specific cell type or environmental conditions

A
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18
Q

A sperm fertilizes an egg and a new individual begins life
1. The sperm and egg must have half the number of chromosomes or else the chromosome number will double with every generation.
2. For now, combination of sperm and egg is the only way to propagate and ensure continuity of the next generation.
3. For variation, there is the need for chromosomes to be able to swap segments or mix to produce different combinations of genes.
4. After gene combination, there is the need for independent assortment of the swapped genes to ensure that further variation is achieved.
5. Thus sexual reproduction was designed to introduce genetic variability to enable us survive the changing environment.
6. In sexually reproducing organisms, meiosis is the type of nuclear division that makes all this possible

Diff between gene combination and independent assortment

A

Great question! Let’s break it down simply:

  1. Gene Combination (Crossing Over):
    • Happens during prophase I of meiosis.
    • Homologous chromosomes pair up and exchange segments of DNA.
    • This mixes genes between maternal and paternal chromosomes.
    • Result: New combinations of alleles on each chromosome.
  2. Independent Assortment:
    • Happens during metaphase I of meiosis.
    • Homologous chromosome pairs line up randomly at the cell’s equator.
    • Each pair separates independently of others.
    • Result: Gametes get different combinations of maternal and paternal chromosomes.

How They’re Related for Variation:
• Crossing over (gene combination) creates new allele combos on a single chromosome.
• Independent assortment ensures that these mixed chromosomes are randomly distributed into gametes.
• Together, they maximize genetic diversity in offspring by producing unique gene combinations every time.

Would you like an MCQ on this to practice?

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19
Q

What phase in meiosis is similar to mitosis?
Why is the prophase of meiosis I divided into five stages? State those stages

Chiasmata (plural of chiasma) are the points where homologous chromosomes physically cross over during prophase I of meiosis. This occurs during crossing over, which is a key process for genetic recombination.

A

Meiosis of eukaryotes
Meiosis requires two nuclear divisions - Meiosis I and Meiosis Il to produce four daughter haploid gamates each having one of each kind of chromosome. Therefore each daughter cell will have half the total number of chromosomes present in the diploid parent nucleus.
Interphase in meiosis is similar to that of mitosis. The Prophase of Meiosis I is divided into 5 stages to ensure genetic arrangement.
Leptotene
Chromosomes, each consisting of two sister chromatids from each parent start condensing into visible strands within the nucleus. At this point, the two sister chromatids are still so tightly bound that they are indistinguishable from one another.

Zygotene
Chromosomes from each parent line up and homologous chromosomes pair up (synapsis) - mechanism unknown. Pairing is highly specific, exact and in perfect alignment. In males the X and Y chromosomes being non homologous line up end to end. Each pair is called bivalent (two chromosomes) or tetrad (four chromatids)

Homologous Chromosomes
• A pair of chromosomes (one from mom, one from dad) that:
• Are same in size and shape
• Have the same genes at the same loci (but can have different alleles)
• Example: Chromosome 1 from mom and Chromosome 1 from dad

Pachytene (most unique in cell division):
Chromosomal crossing over occurs between non-sister chromatids resulting in the exchange of segments over regions of homology a process called genetic recombination. This tightly controlled regional exchange results in recombination of information. The sites where the chromatids are attached is the chiasmata.

Non-Sister Chromatids
• Definition: Chromatids from homologous chromosomes—one from the mother, one from the father.
• Relationship: Same genes, but possibly different alleles.
• Not joined by the same centromere.

And it actually makes sense cuz crossing over occurs between mother and fathers chromatids not mother and mother or father and fathers chromatids

Sister Chromatids
• Definition: Two identical copies of a single chromosome formed by DNA replication.
• Relationship: They are joined together by a centromere.
• Identical? Yes—same genes and same alleles.
• Example: After a chromosome duplicates in S-phase, the two resulting strands are sister chromatids.

Diplotene:
There is a little separation of homologous chromosomes, as they are held tight at the chiasmata points. This enables the homologous chromosomes to locate onto the same spindle.

Diakinesis:
This is the point in meiosis where the homologous chromosomes are visible under the scope especially the chiasmata. The events here are similar to the pro-metaphase stage of mitosis - The nuclear membrane disappears and the spindle begins to form.
In female human development, all developing oocytes stop at diplotene till puberty.

To remember the five stages of Prophase I in meiosis, you can use the mnemonic: “Leaping Zebras Please Dance Daily”, which stands for:
1. Leptotene
2. Zygotene
3. Pachytene
4. Diplotene
5. Diakinesis

Quick Guide to What Happens in Each:
1. Leptotene – Chromosomes start to condense and become visible.
2. Zygotene – Synapsis begins (homologous chromosomes start pairing).
3. Pachytene – Crossing over occurs (exchange of genetic material).
4. Diplotene – Homologs start to separate, but remain connected at chiasmata.
5. Diakinesis – Chromosomes are fully condensed and ready for metaphase.

Want a fun version of the mnemonic too? I can make one with a story or rhyme if you’d like.

Diplotene vs Dictyotene (sometimes spelled dictyate) – both are sub-stages of Prophase I in meiosis, but they differ in what happens and when they occur:

  1. Diplotene
    • Occurs normally during Prophase I.
    • Chiasmata (crossing over points) become visible.
    • Homologous chromosomes start to separate, but stay attached at chiasmata.
    • Happens in both sexes but more emphasized in oogenesis (egg formation).
  2. Dictyotene (Dictyate stage)
    • A prolonged resting phase within Diplotene, specific to female oocytes in humans and some mammals.
    • The cell pauses here and can stay arrested for years (from fetal development until ovulation).
    • During this arrest, the oocyte is maintained in a dormant state until hormonal signals restart meiosis.

In short:
• Diplotene = normal meiotic stage with chiasmata.
• Dictyotene = special resting phase within diplotene, only in female egg cells.

Let me know if you want a quick way to memorize this too!

Here’s a simple explanation of genetic recombination and independent assortment, with a quick comparison at the end:

Genetic Recombination (Crossing Over)
• Occurs in: Prophase I of meiosis.
• What happens?: Non-sister chromatids of homologous chromosomes exchange segments.
• Purpose: Increases genetic variation by creating new combinations of genes not found in either parent.
• Key point: Happens at chiasmata between homologous chromosomes.

Independent Assortment
• Occurs in: Metaphase I of meiosis.
• What happens?: Homologous chromosomes line up randomly at the equator.
• Purpose: Each daughter cell gets a random mix of maternal and paternal chromosomes.
• Key point: Leads to many possible combinations of chromosomes in gametes.

20
Q
  1. Which stage of mitosis is arrested when colcichine, a drug that affects spindle fibre function, is used?
    A. Prophase B. metaphase C. anaphase D. telophase
  2. Which stage is the shortest in mitosis? A. Prometaphase
    B. Anaphase
    C.telophase

Question:
A diploid cell contains 3 pairs of homologous chromosomes. According to the principle of independent assortment, how many possible combinations of chromosomes can be produced in the gametes of this organism (excluding crossing over)?

A. 3
B. 4
C. 6
D. 8

A

Answers are metaphase and anaphase

Here’s the explanation:

The principle of independent assortment states that during meiosis, homologous chromosomes are distributed independently into gametes. Each chromosome pair aligns randomly at the metaphase plate during Metaphase I, meaning each pair has two possible orientations—one chromosome going into one gamete or the other.

So, if an organism has n pairs of chromosomes, the number of possible chromosome combinations due to independent assortment is:

2ⁿ

In this question:
• The cell has 3 pairs of homologous chromosomes.
• Therefore, the number of possible combinations = 2³ = 8

So, D. 8 is correct.

Let me know if you want a visual or analogy to make it easier!

21
Q

Difference between meiosis I and meiosis II and mitosis

A

Meiosis one, homologous chromosomes separate not sister chromatids and it ends up in two daughter cells containing homologous chromosome.Synapsis and
Crossing over occurs here too
Meiosis 2, sister chromatids separate and ends up in 4 daughter cells each containing one sister chromatid

Yes, you’re absolutely right! Let’s break it down with your observations in mind:

Meiosis I: (Reduces chromosome number by half)
• Homologous chromosomes (pairs of chromosomes, one from each parent) separate during anaphase I. This is the key difference from mitosis.
• Synapsis: During prophase I, homologous chromosomes come together in pairs, forming tetrads (four chromatids—two from each homolog).
• Crossing over: Also occurs during prophase I, where homologous chromosomes exchange genetic material, contributing to genetic diversity.
• End result: Two haploid daughter cells, each with half the original chromosome number, but still with two sister chromatids attached to each chromosome.

Meiosis II: (Similar to mitosis but with haploid cells)
• Sister chromatids are separated, just like in mitosis.
• End result: Four haploid daughter cells, each containing only one chromatid from the original homologous pair, resulting in cells with half the chromosome number of the original cell.

Summary:
• Meiosis I: Homologous chromosomes separate (not sister chromatids). The result is two haploid cells, each with two sister chromatids attached to each chromosome.
• Meiosis II: Sister chromatids separate, leading to four haploid daughter cells, each with one chromatid from the original chromosome.

This explains the process of reducing chromosome number in meiosis while generating genetic diversity through crossing over during meiosis I.

Here’s what’s happening in Mitosis:

Let’s say the original diploid cell has 2 chromosomes (1 from mum, 1 from dad = homologous pair).
Before mitosis, these chromosomes duplicate during interphase.
Now you have:
• 2 chromosomes
• Each with 2 sister chromatids
• So a total of 4 chromatids.

During mitosis, those sister chromatids are separated —
But: they go into two cells, not four.

So after division:
• Each daughter cell gets 2 chromosomes (1 chromatid from each original duplicated chromosome).
• Total: 2 daughter cells, each with 2 chromosomes, each chromosome with 1 chromatid.

You started with 2 chromosomes → duplicated to 4 chromatids → then split them evenly into 2 cells.

The main difference between Meiosis I, Meiosis II, and Mitosis lies in the purpose and the number of divisions that occur. Although the steps (Prophase, Metaphase, Anaphase, Telophase) appear similar, they are part of different processes with different outcomes. Let’s break it down:

Meiosis I (Reductional Division)
• Goal: Reduces chromosome number by half to create haploid cells (cells with half the original chromosome number).
• Key difference: Homologous chromosomes (pairs from mom and dad) are separated, not sister chromatids.

Key events in Meiosis I:
• Prophase I: Chromosomes condense, homologous chromosomes pair up, and crossing over occurs (exchange of genetic material between homologs).
• Metaphase I: Homologous chromosomes align at the metaphase plate in pairs (not individual chromosomes).
• Anaphase I: The homologous chromosomes (one from each parent) are pulled to opposite poles, not sister chromatids. The sister chromatids stay attached.
• Telophase I: The cell divides into two haploid daughter cells. Each daughter cell has one set of chromosomes, but the chromosomes still consist of two sister chromatids.

Meiosis II (Equational Division)
• Goal: Separates the sister chromatids of each chromosome to produce haploid cells (similar to mitosis, but starting with haploid cells from Meiosis I).
• Key difference: Just like mitosis, the chromosomes line up, and sister chromatids are separated. But the starting cells are haploid instead of diploid.

Key events in Meiosis II:
• Prophase II: Chromosomes condense, and spindle fibers form in each haploid cell. There’s no crossing over because no homologous chromosomes are present (the chromosomes are already separated).
• Metaphase II: Chromosomes (each consisting of two sister chromatids) align along the metaphase plate.
• Anaphase II: Sister chromatids are pulled apart to opposite poles, creating individual chromosomes.
• Telophase II: The cells divide into four haploid daughter cells, each with a single chromatid (making a total of four genetically diverse cells).

Mitosis (Regular Cell Division)
• Goal: Produces two genetically identical diploid cells (same chromosome number as the parent cell).

Key events in Mitosis:
• Prophase: Chromosomes condense and spindle fibers form.
• Metaphase: Chromosomes line up along the metaphase plate (individual chromosomes).
• Anaphase: Sister chromatids are pulled apart to opposite poles.
• Telophase: Cytokinesis occurs, and two identical daughter cells are formed.

Summary of the Differences:
1. Meiosis I:
• Homologous chromosomes are separated.
• Reduces chromosome number by half.
• Results in two haploid daughter cells.
2. Meiosis II:
• Similar to mitosis.
• Separates sister chromatids.
• Results in four haploid daughter cells.
3. Mitosis:
• Separates sister chromatids.
• Results in two diploid daughter cells (same chromosome number as the parent).

In short:
• Meiosis I is the reduction division where the chromosome number is halved (separating homologous chromosomes).
• Meiosis II is similar to mitosis but starts with haploid cells, and it separates sister chromatids.
• Mitosis separates sister chromatids and creates two genetically identical diploid cells.

Hope this helps clarify!

22
Q

Who discovered mitosis and who discovered meiosis?
In meiosis, There is at least one crossing-over or DNA exchange per homologous pair of chromosomes.

In mitosis-The centromeres split during anaphase
In meiosis-The centromeres do separate during anaphase II, but not during anaphase I.

In mitosis: The genotype of the daughter cells is identical to that of the mother cells.
In meiosis: Meiotic products differ in their genotype from the mother cell.

In mitosis: After mitosis, each daughter cell has exactly same DNA strands

In meiosis: After meiosis, each daughter cell has only half of the DNA strands

Thanks for pointing that out—you’re absolutely right.

Let’s go step-by-step to ensure every single sentence from your oogenesis and spermatogenesis notes is transformed into MCQs. Here’s what you originally wrote, broken down with exact ideas converted into questions:

  1. Oogenesis:Diploid oogonia divide to produce primary oocytes by third month of fetal development and then suspended.
    MCQ:
    At what stage is oogenesis suspended during fetal development?
    A. Metaphase I
    B. Diplotene of Prophase I
    C. Anaphase I
    D. Telophase IIMeiosis continues after puberty.
    MCQ:
    When does oogenesis resume after its fetal suspension?
    A. At birth
    B. At puberty
    C. At ovulation
    D. After fertilizationIn meiosis I, the primary oocyte produces one secondary oocyte and one polar body (nothing can be done with this).
    MCQ:
    The product of meiosis I in oogenesis is:
    A. Two ovum cells
    B. One secondary oocyte and one polar body
    C. Two polar bodies
    D. One zygoteThe secondary oocyte with all the cytoplasm proceeds down the fallopian tube and the polar body dies off.
    MCQ:
    What happens to the cytoplasm during meiosis I in oogenesis?
    A. It’s evenly divided between the daughter cells
    B. Most cytoplasm goes to the secondary oocyte
    C. All cytoplasm is lost
    D. It forms a zygote immediatelyMeiosis II begins after fertilization to form a matured ovum and another polar body.
    MCQ:
    When is meiosis II of oogenesis completed?
    A. Before puberty
    B. At ovulation
    C. After fertilization
    D. After menstruationThen one hour after fertilization, the nuclei of sperm and egg fuse to form the diploid zygote.
    MCQ:
    When does the zygote form in human fertilization?
    A. Immediately after sperm entry
    B. About one hour after fertilization
    C. During ovulation
    D. After meiosis I
  2. Spermatogenesis:Seminiferous tubules have spermatogonia (2n).
    MCQ:
    Where are spermatogonia found in males?
    A. Epididymis
    B. Seminiferous tubules
    C. Vas deferens
    D. ProstateMitosis to produce primary spermatocytes (2n).
    MCQ:
    What type of division gives rise to primary spermatocytes from spermatogonia?
    A. Meiosis I
    B. Mitosis
    C. Binary fission
    D. FertilizationThen meiosis I to produce secondary spermatocytes, then meiosis II to produce spermatids (1n).
    MCQ:
    The correct order in spermatogenesis is:
    A. Spermatogonia → Secondary spermatocyte → Primary spermatocyte → Spermatid
    B. Spermatogonia → Primary spermatocyte → Secondary spermatocyte → Spermatid
    C. Spermatid → Secondary spermatocyte → Primary spermatocyte
    D. Primary spermatocyte → Spermatogonia → SpermatidSpermatids lose cytoplasm and develop tails for locomotion to become sperms.
    MCQ:
    What change transforms spermatids into mature sperm cells?
    A. Cytoplasm division and chromatin expansion
    B. Cytoplasm loss and tail development
    C. Tail shortening and nucleus removal
    D. Head enlargement and tail lossThis process is continuous in man.
    MCQ:
    Which of the following is true about spermatogenesis in men?
    A. It occurs only in fetal life
    B. It halts at puberty
    C. It is continuous after puberty
    D. It occurs once in a lifetime

Let me know if you’d like the correct answers and explanations for these as well—or if you’d prefer them exported into a file or study format like flashcards or CSV.

Oogenesis: Paused twice:
• Prophase I (diplotene) – from fetal development until puberty
• Metaphase II – resumes only at fertilization

A

Mitosis: Oscar Hertwig
Meiosis: Walther Fleming

Great! Here’s the full set of MCQs with answers and explanations for each, covering every sentence from your notes:

Oogenesis
1. At what stage is oogenesis suspended during fetal development?
Answer: B. Diplotene of Prophase I
Explanation: By the third month of fetal development, primary oocytes are formed and arrested in diplotene of prophase I until puberty.

Great question!

In oogenesis, meiosis pauses at Metaphase II to wait for fertilization.

Here’s why:
• The secondary oocyte is arrested at Metaphase II after ovulation.
• It only completes meiosis II if a sperm fertilizes it.
• This arrest ensures the egg doesn’t waste energy or divide unnecessarily unless fertilization actually happens.

The biological reason:
• The metaphase II arrest is controlled by a complex called the cytostatic factor (CSF) which holds the cell in that stage.
• Once a sperm penetrates the oocyte, a rise in intracellular calcium triggers the egg to exit metaphase II and complete meiosis, forming the mature ovum and a second polar body.

Summary:
• Paused at Metaphase II to wait for sperm.
• Resumes only at fertilization.

Would you like a diagram or short memory aid to help remember this?

Excellent follow-up!

Here’s why meiosis halts specifically at Metaphase II in oogenesis:

  1. Metaphase II is the last checkpoint before final division
    • By the time the oocyte reaches Metaphase II, it has already halved its chromosome number.
    • All that’s left is to separate the sister chromatids.
    • This is the final irreversible step, and once completed, the egg becomes a haploid mature ovum.
  2. Holding at Metaphase II prevents waste
    • Completing meiosis without fertilization would mean the oocyte fully matures but has no sperm to fuse with.
    • That would be a waste of energy and resources—especially since females are born with a fixed number of eggs.
    • So the body waits at Metaphase II, just before the final split, to ensure it’s needed.
  3. Fertilization triggers the “go-ahead”
    • The presence of sperm signals the oocyte to complete meiosis II.
    • This ensures that the egg is matured only when it’s truly needed—i.e., when it’s about to become part of a zygote.

Easy analogy:

It’s like standing at the door before stepping onto a stage. You only step out (finish meiosis) if the audience (sperm) shows up.

Want this in a short one-line memory version?

2.	When does oogenesis resume after its fetal suspension? Answer: B. At puberty Explanation: The arrested primary oocytes resume meiosis I at puberty during each menstrual cycle.
3.	The product of meiosis I in oogenesis is: Answer: B. One secondary oocyte and one polar body Explanation: Meiosis I results in unequal cytoplasmic division: one large secondary oocyte and one small polar body.
4.	What happens to the cytoplasm during meiosis I in oogenesis? Answer: B. Most cytoplasm goes to the secondary oocyte Explanation: Almost all the cytoplasm is retained in the secondary oocyte; the polar body gets minimal cytoplasm and later degenerates.
5.	When is meiosis II of oogenesis completed? Answer: C. After fertilization Explanation: Meiosis II only completes if fertilization occurs, producing a mature ovum and a second polar body.
6.	When does the zygote form in human fertilization? Answer: B. About one hour after fertilization Explanation: After fertilization triggers completion of meiosis II, the nuclei of sperm and ovum fuse within about an hour, forming a diploid zygote.

Spermatogenesis
7. Where are spermatogonia found in males?
Answer: B. Seminiferous tubules
Explanation: Spermatogonia are diploid stem cells located in the seminiferous tubules of the testes.
8. What type of division gives rise to primary spermatocytes from spermatogonia?
Answer: B. Mitosis
Explanation: Spermatogonia undergo mitosis to produce primary spermatocytes, which then enter meiosis.
9. The correct order in spermatogenesis is:
Answer: B. Spermatogonia → Primary spermatocyte → Secondary spermatocyte → Spermatid
Explanation: This is the correct sequence: mitosis forms primary spermatocytes (2n), meiosis I forms secondary spermatocytes, and meiosis II forms spermatids (1n).
10. What change transforms spermatids into mature sperm cells?
Answer: B. Cytoplasm loss and tail development
Explanation: Spermatids undergo structural changes including loss of excess cytoplasm and formation of flagella (tails) to become spermatozoa.
11. Which of the following is true about spermatogenesis in men?
Answer: C. It is continuous after puberty
Explanation: Unlike oogenesis, spermatogenesis continues uninterrupted from puberty throughout a man’s life.

Let me know if you’d like these compiled into a printable or flashcard-friendly format!

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Q

Great question!

Independent assortment and independent segregation are closely related, but not exactly the same:

  1. Independent Assortment

This is the principle that:
• During Metaphase I of meiosis, homologous chromosome pairs line up randomly at the equator.
• This leads to different combinations of maternal and paternal chromosomes in the gametes.

Example:
If you have 3 chromosome pairs, you get 2³ = 8 possible combinations of chromosomes in the gametes.

  1. Independent Segregation

This term is sometimes used interchangeably, but it actually refers more specifically to:
• The separation (segregation) of the alleles (gene versions) during meiosis.
• Each allele in a pair segregates independently into different gametes.

In short:
• Independent assortment: Focuses on chromosome behavior (how they randomly arrange).
• Independent segregation: Focuses on allele behavior (how gene copies go into gametes).

But in practice, many use the terms interchangeably—especially in simpler discussions—because both lead to genetic variation.

Want a memory trick to keep them apart?

Sure! Let’s break it down simply and clearly:

Connecting Concepts – Cell Division

Cell division is how our body grows, heals, and replaces old cells. But it must be carefully controlled. If this control is lost, problems occur:

  1. Psoriasis:
    • What happens: The cell cycle speeds up too much.
    • Result: Too many skin cells are made, leading to thick, scaly skin patches.
    • Takeaway: Overstimulation causes overproduction of tissue.
  2. Underproduction (Early Cell Death):
    • If the cell cycle is too slow or cells die too early, not enough cells are produced.
    • This can cause issues like organ failure or slow healing.
  3. Cancer:
    • The worst-case scenario of cell cycle gone wrong.
    • Cells divide uncontrollably because:
    • Signals that tell cells to stop aren’t received or ignored.
    • The body loses control over growth.
    • Like a company where workers ignore instructions — things fall apart.
  4. Tissue Engineering:
    • Scientists can manipulate the cell cycle to:
    • Grow tissues for transplants.
    • Clone food (like meat) in labs.
    • Make things faster and cheaper than competitors.
  5. Absolute Control:
    • If we master the cell cycle completely:
    • We could cure many genetic diseases.
    • Help people reach peak physical health.
    • Extend life and improve quality of life.

Summary:

Controlled cell division = health.
Uncontrolled or poorly timed division = disease or disorder.
Harnessed control = powerful medical and industrial benefits.

Want a visual diagram to go with this?

24
Q

What is terminalization?

I. Terminalization
• After crossing over, the chiasmata (the X-shaped regions where crossing over occurred) move toward the chromosome ends — this is terminalization.

Question 3
In which phase of the cell cycle are the chromosomes inactive, condensed, and not transcribed to messenger RNA?
A.G1 phase
B.G2 Phase
C.M phase
D.S phase

At the metaphase plate during metaphase II of meiosis, there are
A.Bivalents or tetrads
B.Chromosomes consisting of one chromatid
C.Homologous pairs of chromosomes
D.Unpaired duplicated chromosome

A

Question 1

In which phase of the cell cycle are the chromosomes inactive, condensed, and not transcribed to messenger RNA?
Correct Answer: C. M phase

Explanation:
• The M phase (mitosis or meiosis) is when the chromosomes are most condensed.
• Condensed DNA prevents transcription, so mRNA is not produced.
• This makes the chromosomes inactive during this phase.
• G1, S, and G2 phases all involve some level of gene expression or DNA activity.

Question 2

At the metaphase plate during metaphase II of meiosis, there are
Correct Answer: D. Unpaired duplicated chromosome

Explanation:
• Metaphase II happens after homologous chromosomes have already been separated in Meiosis I.
• Now, individual chromosomes line up, each made of two sister chromatids — this is a duplicated chromosome.
• They are not paired with homologs, so they are unpaired duplicated chromosomes.

Let me know if you’d like similar MCQs with Bible references or diagrams!

Great question — let’s go step by step to clear this up:

Why are chromosomes duplicated at metaphase II?

Because DNA replication happens only once, during S phase (before meiosis I starts).
• In meiosis I, homologous chromosomes separate — but sister chromatids stay together.
• That means the cells entering meiosis II still have duplicated chromosomes (each with two sister chromatids).
• So at metaphase II, these duplicated chromosomes line up at the equator — one chromatid on each side, connected at the centromere.

You’re right:

There are chromatids at each end held by spindle fibers at the centromere.

Exactly! That centromere is still intact in metaphase II — it hasn’t split yet. So the chromosome is still duplicated (2 sister chromatids).

What happens after metaphase II?

In anaphase II, the centromere splits, and the sister chromatids are pulled apart to opposite poles — now each one becomes an individual unduplicated chromosome.

So in short:
• Metaphase II: duplicated chromosomes (2 chromatids each)
• Anaphase II: chromatids separate
• After meiosis II: 4 cells, each with unduplicated chromosomes

Would you like a visual or a quick analogy to help lock it in?

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Valid feature(s) of gastrulation include(s) 1. The epiblast forms the mesoderm Il. The extraembryonic mesoderm is formed by the endoderm III. The primitive streak is the source of epithelial-mesenchymal transition IV. Commences from primitive node 1, II and Ill only I and Ill only I, III and IV only I, II, Ill and IV Valid feature(s) of folding include(s) 1. Head fold moves the heart to a ventrocaudal position Il. Tail folding causes the cloaca membrane to move ventracaudally III. Lateral fold incorporates the umbilical cord completely as midgut I and Il only I and Ill only Il and III only I, Il and III Q1 The valid features observed in the day 8 of development include(s) 1. Amnioblast has formed II. Implantation is completed Ill. The bilaminar disc has formed IV. The chorionic cavity has formed I and II only I and III only I, Ill and IV only 1, 11, III and IV 12. all the following are numerical anomalies except a. Cri du chat b.Klinefelter? c. Patau d. Turner’s
Correct answer: III. I, III and IV only Explanation: Let’s evaluate each statement: I. The epiblast forms the mesoderm True – During gastrulation, cells from the epiblast migrate through the primitive streak to form mesoderm and endoderm. II. The extraembryonic mesoderm is formed by the endoderm False – Extraembryonic mesoderm is not derived from the endoderm. Its origin is debated, but it’s generally considered to come from the epiblast or yolk sac, not the endoderm. III. The primitive streak is the source of epithelial-mesenchymal transition (EMT) True – Cells undergoing EMT migrate through the primitive streak to form mesoderm and endoderm. IV. Commences from primitive node True – Gastrulation starts at the primitive node, also called Hensen’s node. Summary: • I = True • II = False • III = True • IV = True Answer: I, III and IV only Folding Question Correct answer: I and II only Explanation of each statement: I. Head fold moves the heart to a ventrocaudal position True – The head fold brings the developing heart from a cranial position to a ventral and caudal position relative to the head. II. Tail folding causes the cloacal membrane to move ventrocaudally True – Tail folding shifts the cloacal membrane ventrally and caudally, positioning it appropriately for future development. III. Lateral fold incorporates the umbilical cord completely as midgut False – Lateral folding incorporates the yolk sac into the embryo as the gut, but the umbilical cord is not incorporated as midgut. It remains as an external structure containing the connecting stalk, allantois, and yolk sac remnants. Sure! In embryology, “folding” refers to the process during the 4th week of development that transforms the flat trilaminar embryonic disc into a three-dimensional structure resembling a human body. This happens through two major types of folding: 1. Longitudinal Folding (Head and Tail Folds) Also called cranio-caudal folding • Head Fold: • Caused by rapid growth of the neural tube (brain region). • Moves: • Oropharyngeal membrane and developing heart ventrally (to the front) and caudally (downward). • Septum transversum (future diaphragm) comes to lie between thorax and abdomen. • Tail Fold: • Caused by growth at the caudal end (near the primitive streak). • Moves: • Cloacal membrane ventrally and cranially. • Connecting stalk (future umbilical cord) becomes positioned at the ventral side of the embryo. 2. Transverse Folding (Lateral Folding) • Caused by rapid growth of the somites and lateral edges of the disc. • Brings the right and left sides of the embryo together at the midline. • Fuses to form: • The ventral body wall. • Incorporates part of the yolk sac into the embryo as the primitive gut (midgut). • Also results in formation of the intraembryonic coelom (future body cavities). Summary Table: Type of Folding Direction Key Results Head Fold Cranial to ventrocaudal Heart and oropharyngeal membrane move ventrally Tail Fold Caudal to ventrocranial Cloacal membrane and connecting stalk repositioned Lateral Fold Right/left sides to midline Formation of body wall, gut tube, and cavities Let me know if you want diagrams, a quiz, or flashcards based on this! Great question! What are somites? Somites are blocks of mesodermal tissue that form in pairs on either side of the neural tube during early embryonic development. They are segmented structures and play a major role in forming important parts of the body. Where are they? • Somites form along the longitudinal axis of the embryo, on both sides of the notochord and neural tube, from the head region down to the tail. • You can think of them as little “chunks” or “segments” lined up like a train track on each side of the spine. What do somites become? Each somite differentiates into 3 key parts: 1. Sclerotome → Vertebrae and ribs 2. Dermatome → Dermis of the skin (especially back skin) 3. Myotome → Skeletal muscles (especially of the back, body wall, and limbs) When do they appear? • Somites start forming around day 20 of development. • By the end of the 5th week, there are usually around 42–44 pairs of somites. Quick Summary: Somite Part Future Structure Sclerotome Vertebrae, ribs Myotome Skeletal muscles Dermatome Dermis (skin) Let me know if you’d like a simple diagram or memory trick! Day 8 of Development Question Correct answer: I and III only Explanation of each statement: I. Amnioblast has formed True – Amnioblasts line the amniotic cavity by day 8. II. Implantation is completed False – Implantation is still ongoing on day 8 and is typically completed around day 9. III. The bilaminar disc has formed True – At day 8, the epiblast and hypoblast form the bilaminar embryonic disc. IV. The chorionic cavity has formed False – The chorionic cavity (extraembryonic coelom) begins forming later, around day 12. Let me know if you want an MCQ version with distractors and explanations! 12. Correct answer: a. Cri du chat Explanation: Numerical anomalies involve changes in the number of chromosomes (extra or missing chromosomes). Structural anomalies involve deletions, duplications, inversions, or translocations in chromosome structure. Let’s go through each: a. Cri du chat – Not a numerical anomaly • It is a structural anomaly caused by a deletion on the short arm of chromosome 5 (5p deletion). • Characterized by a high-pitched cry (like a cat), intellectual disability, and facial abnormalities. b. Klinefelter syndrome – Numerical anomaly • Caused by an extra X chromosome in males: 47,XXY c. Patau syndrome – Numerical anomaly • Caused by trisomy 13: 47,XX+13 or 47,XY+13 d. Turner’s syndrome – Numerical anomaly • Caused by missing one X chromosome in females: 45,X Summary: Only Cri du chat is not due to abnormal chromosome number, so it’s the correct answer. Nullisomy is the aneuploid condition in which two homologous chromosomes are missing, so that the organism has 2n – 2 chromosomes. Monosomy refers to the absence of a single chromosome, giving 2n – 1 total chromosomes. In trisomy, one extra chromosome is present (2n + 1). Aneuploidy refers to a condition where a cell has an abnormal number of chromosomes, such as having an extra chromosome (trisomy) or a missing chromosome (monosomy). Polyploidy, on the other hand, is a state where an organism has more than two complete sets of chromosomes.
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The key mechanistic failure in patients with xeroderma pigmentosum involves which of the following? (A) Mutation in the primase gene (B) Inability to excise a section of the UV-damaged DNA (C) Mutation of one of the mismatch repair components (D) Inability to synthesize DNA across the damaged region (E) Loss of proofreading capacity d.   9. Lysine is a. wholly ketogenic b. wholly glucogenic c. keto glucogenic d. an acidic amino acid Which of the following is responsible for retaining the enzyme protein disulfide isomerase in the ER? (A) Glycosylation (B) The presence of a KDEL sequence at the C-terminal (C) Retention of the signal peptide (D) Phosphorylation of Ser 22 (E) Attachment of a fatty acid What feature of the compounds in a racemic mixture is absent? A. Mutarotation B. Optical activ Which of the following does not affect membrane potential? A. Osmolarity B. Osmolality C. Separation of charges D. Conductance of membrane   23. Which  of the following is a table sugar ? A.reducing oligosaccharide B.non-reducing sugar C.Lactose and maltose 19.A student left a solution of glucose in a lab overnight. The next day, he found traces of mannose and galactose in the solution. Which of the following likely explains the observation? A. It is a natural occurrence of sugars B. He might have accidentally added an acid to the solution C. He might have accidentally added a base to the solution   20. Which of the following determines the quaternary structure of a protein? A. Number of peptide bonds B. Amino acid composition C. Amino acid sequence D. Number of polypeptide 1.When a chemical splashes in your eye what should you do A.neutralize it B.immediately wash it off C.use a cloth to wash it off   2. What happens when there’s a fire in the lab A. Use a fire extinguisher and seek help B. Do nothing   3. When should you wear your lab coat to the lab? A.when you feel like it B. Always C. Only when you’re working   4. A person with Zellweger disease will have empty peroxisomes. Which of the following will be a sign in the patient A. Inability to detoxify alcohol B. Low ATP production C. An increase in short fatty acid chains   5. What is the junction between the epithelium and the basement membrane   6. Something about the muscles affecting by alvusion of muscles on the greater tubercule I. Lateral rotation II. Medial rotation III. Abduction   7. What carbon atom of a carbohydrate must be changed in order to convert it between it's D and L forms A. Penultimate carbon B. Last carbon with OH C. Chiral center   8. The effect, on a young adult male, of the loss of 1.5 liters body water will be a/an A. decrease in osmolarity B. decrease in plasma osmolarity C. increase in plasma osmolarity D. increase in volume of ECF   9. Which of the following has sphingol as the alcohol group? A. Ganglioside B. Phosphatidyl inositol   10. A man was doing an exercise and suddenly felt a sharp pain at the shoulder joint. An examination revealed that a muscle attached to the lateral lip of the intertubercular sulcus has been torn. Which of the following movements is affected? I adduction II extension III Medial rotation A. III only B. I, II III C. III D. II, III   11. The cation that when in excess can cause an increase in extra cellular fluid is A.Potassium B.Chlorine C.Sodium   12. The muscle attached to the floor of the inter tubercular groove is A.Latissimus dorsi B.Pectoralis major C.Teres minor   13. After running a marathon, the athlete collapsed. What could be the possible reason for this? A. Increase in plasma osmolality B. Over intake of water C. Excess loss of sodium ions through sweat D. Low production of ADH   14. The suprasponous nerve innervation is I. From The posterior cord II. from  Superior trunk   15. Something about  how NADPH protects red blood cells A. Reduced glutathione B. Disulfide bridges   16. Which of the following is not found in the quartenary structure of proteins A. Peptide bond B. Hydrogen bonds C. Metal ions D. Salt bridge   17. Polymerization of macromolecules involves which of the ff bonds A. Glycosidic bond B. Polypeptide bond C. Ionic bond D. Covalent bond   18. The enzyme Glucose-6-phosphate dehydrogenase catalyzes which step in the PPP
Here are the correct answers and explanations: 1. Xeroderma Pigmentosum — Key Mechanistic Failure Correct Answer: (B) Inability to excise a section of the UV-damaged DNA Explanation: Xeroderma pigmentosum is caused by a defect in the nucleotide excision repair (NER) pathway, which normally removes UV-induced thymine dimers. These patients cannot excise damaged DNA segments, leading to mutation accumulation and skin cancer. 2. Lysine is… Correct Answer: (a) Wholly ketogenic Explanation: Lysine and leucine are the only amino acids that are exclusively ketogenic, meaning their catabolism yields ketone bodies, not glucose. The amino acids that are both ketogenic and glucogenic are: • Isoleucine • Phenylalanine • Tryptophan • Tyrosine • Threonine Mnemonic: “PITTT” Phenylalanine Isoleucine Tryptophan Tyrosine Threonine These amino acids can produce both: • Glucose (via intermediates like pyruvate or TCA cycle components) • Ketone bodies (via acetyl-CoA or acetoacetate) Let me know if you want a mnemonic for the purely ketogenic or purely glucogenic ones too! 3. Retaining protein disulfide isomerase in the ER Correct Answer: (B) The presence of a KDEL sequence at the C-terminal Explanation: The KDEL sequence (Lys-Asp-Glu-Leu) acts as a retrieval signal to keep certain proteins, like protein disulfide isomerase, within the endoplasmic reticulum. 4. Feature absent in a racemic mixture Correct Answer: B. Optical activity Explanation: A racemic mixture has equal amounts of both enantiomers, so their optical rotations cancel out — the solution has no net optical activity. 5. Which does NOT affect membrane potential? Correct Answer: A. Osmolarity Explanation: Membrane potential is affected by ion concentration gradients, charge separation, and membrane conductance, but not directly by osmolarity, which affects water movement, not voltage. 6. Which of the following is a table sugar? Correct Answer: B. Non-reducing sugar Explanation: Table sugar = sucrose, which is non-reducing because its anomeric carbons are involved in the glycosidic bond, preventing ring opening and reduction. 7. Glucose turning into mannose and galactose overnight Correct Answer: C. He might have accidentally added a base to the solution Explanation: In alkaline conditions, glucose can undergo epimerization and isomerization, forming mannose and galactose. 8. What determines quaternary structure? Correct Answer: D. Number of polypeptide chains Explanation: The quaternary structure refers to the arrangement of multiple polypeptide subunits in a protein complex. Let me know if you’d like flashcards or mnemonics to help with any of these! That’s a solid and detailed list of exam questions. Let’s go through the answers and brief explanations for each to help you revise effectively: 1. Chemical in eye: B. Immediately wash it off • Always flush with water immediately to prevent chemical burns. 2. Fire in lab: A. Use a fire extinguisher and seek help • Safety first—act quickly and inform others. 3. Lab coat use: B. Always • Essential PPE in the lab environment. 4. Zellweger disease sign: C. An increase in short fatty acid chains • Peroxisomes break down very long-chain fatty acids. In Zellweger, this doesn’t occur. 5. Junction between epithelium and basement membrane: Basal lamina (not given as options here, but that’s the correct term). 6. Greater tubercle muscle avulsion affects: I. Lateral rotation, III. Abduction • Supraspinatus (abduction), Infraspinatus and Teres minor (lateral rotation) attach there. 7. D and L forms of carbohydrates: A. Penultimate carbon • The second-to-last carbon determines D or L. 8. Loss of 1.5 L of water: C. Increase in plasma osmolarity • Water loss concentrates the solutes in plasma. 9. Sphingol alcohol group: A. Ganglioside • Sphingolipids have sphingosine as their backbone. 10. Muscle torn at lateral lip of intertubercular sulcus: B. I, II, III • Pectoralis major is involved in adduction, extension, and medial rotation. 11. Cation that increases ECF: C. Sodium • Sodium is the main ECF ion, and water follows it osmotically. 12. Muscle at floor of intertubercular groove: A. Latissimus dorsi 13. Athlete collapse after marathon: C. Excess loss of sodium ions through sweat • This leads to hyponatremia and collapse. 14. Suprascapular nerve innervation: II. From the superior trunk 15. How NADPH protects RBCs: A. Reduced glutathione • NADPH regenerates reduced glutathione, which protects against oxidative damage. 16. Not in quaternary structure: A. Peptide bond • Peptide bonds are found in primary structure. 17. Macromolecule polymerization bond: D. Covalent bond • All macromolecules are joined by covalent bonds (e.g., peptide, glycosidic). 18. G6PD enzyme in PPP: • It catalyzes the first step, converting glucose-6-phosphate to 6-phosphogluconolactone and producing NADPH. If you’d like me to split these into flashcards or convert them into multiple-choice quizzes, just let me know!
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The cell is not only a structural unit but also a functional unit of organs. Thus in illnesses such as diabetes or prostrate cancer, it is the cells of the pancreas or the prostrate that are malfunctioning, and not the organ. Every cell comes from a pre-existing cell, and do not arise on their own accord. ➢Cells are very small because they need a surface area that can adequately exchange material with the environment. Large cells will have difficulty moving materials effectively within the cytoplasm. Note; tubulin filaments is the spindle fibers Cytokinesis uses actin filaments DNA. It consists of a semi-fluid matrix called cytosol into which the other components of the cell bath. Note that cells are self sustaining. as it has the ability to acquire nutrients to be processed into required cellular constituents for use and excrete waste and toxic materials across the barrier to the outside. Note: 1mm is the minimum resolution the eye should be able to see. Anything that can’t scatter light, you won’t be able to see it.
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microscopes These microscopes uses visible light waves to pass through the cell. The light waves are bent by the cells and brought into focus by a set of glasses which enlarge these parts. Light microscopes can magnify up to about 2000X. Cell parts that are smaller than the light wavelengths cannot bend the light rays and they become blurred to the eye. Electron microscopes Electron wavelengths are 100,000 shorter than visible light, and very thin parts of cells can bend them. Thus they can magnify up to 100,000X more than light microscopes. Electrons cannot pass through glass so they are bent and brought into focus by magnetic lenses. Since human eye cannot use electrons to see, images are focused onto a screen. Note that light microscope is used to view living organisms that’s why change in shape of a living blood cell you can use light microscope for it. You use electron microscope for dead things. Scanning Electron Microscope (SEM) – The electron beams moves back and forth the surface of the specimen which has thin coating of metal. The response by the metal is converted to an image of the surface Great question! SEM (Scanning Electron Microscopy) is important even though it only shows surface structures because: 1. Detailed 3D Surface View: SEM gives high-resolution, 3D-like images of the surface of cells, tissues, or materials. This is super useful in fields like biology, materials science, and forensics where surface details matter. 2. Texture and Morphology: It reveals texture, shape, and structure—important for identifying bacteria, tissue abnormalities, nanomaterials, or even manufacturing defects. 3. Elemental Analysis: With accessories like EDX (Energy Dispersive X-ray), SEM can also identify the elements present on the surface. So even though it doesn’t show internal structures, it’s crucial for analyzing outer morphology, quality control, and detecting surface-level changes or defects. Note : For prokaryotes- A single intracellular compartment surrounded by the plasma membrane. 6.The cytoplasm has many ribosomes for protein synthesis. DNA is concentrated in a region of the cytoplasm called the nucleoid. Prokaryotic cells inherit one molecule of circular DNA and small accessory rings of DNA called plasmids. Many disease causing bacteria have thick antigenic jellylike polysaccharides around their capsules. Here are some MCQs based on your text about the nucleus: 1. What is the semifluid medium inside the nucleus called? A. Cytoplasm B. Nucleoplasm C. Chromatin D. Riboplasm Answer: B. Nucleoplasm Explanation: The nucleoplasm is the semifluid substance within the nucleus that suspends chromatin and other nuclear components. 2. What is chromatin composed of? A. DNA and RNA B. DNA and proteins (histones) C. RNA and lipids D. Ribosomes and proteins Answer: B. DNA and proteins (histones) Explanation: Chromatin is made of DNA wrapped around histone proteins. 3. What is the function of the nucleolus? A. DNA replication B. Protein synthesis C. rRNA synthesis and ribosome assembly D. Lipid production Answer: C. rRNA synthesis and ribosome assembly Explanation: The nucleolus is responsible for producing ribosomal RNA and assembling ribosomes. 4. What allows materials to move in and out of the nucleus? A. Endoplasmic reticulum B. Mitochondria C. Nuclear pores D. Vesicles Answer: C. Nuclear pores Explanation: Nuclear pores regulate the exchange of materials between the nucleus and cytoplasm. 5. What is the role of importin and exportin? A. Ribosome synthesis B. Controlling gene expression C. Transport of molecules through nuclear pores D. Synthesizing DNA Answer: C. Transport of molecules through nuclear pores Explanation: Importin and exportin are binding proteins that help control what enters and exits the nucleus through nuclear pores. 6. Which of the following is not a function of the nucleus? A. Isolating DNA from cytoplasmic activity B. Synthesizing lipids C. Controlling access to DNA D. Providing environment for DNA and RNA synthesis Answer: B. Synthesizing lipids Explanation: Lipid synthesis occurs in the smooth ER, not in the nucleus. Let me know if you’d like these in printable format or as flashcards! 7. What separates the nucleus from the cytoplasm? A. Nuclear pores B. Ribosomes C. The nuclear envelope D. Golgi apparatus Answer: C. The nuclear envelope 8. Which of the following does NOT occur at the nuclear pores? A. Exit of ribosomes B. Entry of proteins for DNA replication C. mRNA transport D. Fatty acid synthesis Answer: D. Fatty acid synthesis 9. Which of these is not one of the three main functions of the nucleus? A. DNA protection from cytoplasmic damage B. Lipid synthesis C. Regulated access to DNA D. Environment for nucleic acid synthesis Answer: B. Lipid synthesis Ribosomes are formed in the nucleolus. Rrna plus proteins gives you ribosomes
The Nucleus - Information Central The nucleus contains chromatin in a semifluid medium called the nucleoplasm. Chromatin is the name for the collection of DNA and proteins (histones) in the nucleus of eukaryotes. Within the nucleus is a dark region called the nucleolus where ribosomal RNA (rRNA) are synthesized and where RNA joins with proteins to form ribosomes. The nucleus is separated from the cytoplasm by the nuclear envelope made of two membranes. There are nuclear pores tightly controlled by binding proteins called importin and exportin. These pores allow synthesized ribosomes to leave and attach to the ER, allows the modified mRNA after transcription to travel to the cytoplasm for protein synthesis and allows proteins required for replication, repair and other processes to enter. The nucleus has three functions - (i) It isolates the cell's DNA from potentially damaging reactions in the cytoplasm and ii) its nuclear membrane allows restricted access to the DNAs hereditary information through controls over receptors, transport proteins and pores at its surface and iii) provides the environment for the synthesis of DNA, RNA and ribosomes. Mcqs
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What are polyribosomes and when will a ribosome bind to the ER? Between bound and free ribosomes, which produce functional proteins?
In eukaryotes, some ribosomes occur freely in the cytoplasm either singly or in groups called polyribosomes(free ribosomes that are in clusters) . Bound and free ribosomes are identical Proteins from free ribosomes function in the cytosol e.g. glycolytic enzymes and proteins from bound ribosomes are destined for modification and packaging before export to its final destination. A ribosome will bind to the endoplasmic reticulum (ER) if the protein it will synthesize has an ER sequence. An ER sequence (also called a signal sequence or signal peptide) is a short stretch of amino acids at the beginning of a newly made protein that tells the ribosome: “Send me to the Endoplasmic Reticulum (ER)!” In simple terms: • It’s like a postal code or shipping label. • The ribosome reads it early during translation. • If the protein has an ER signal, the ribosome attaches to the rough ER and continues making the protein into the ER lumen. Free ribosomes produce functional proteins. Rough ER ribosomes doesn’t produce functional proteins. They produce proteins that need to be modified before they can be functional. Once the proteins form, they enter the ER. After these ribosomes make the initial (immature) protein, the protein: • Enters the lumen of the rough ER, where it undergoes modification (like folding, adding sugars, etc.). • Then it’s sent to the Golgi apparatus for further processing, sorting, and packaging. • After that, it’s ready to go to its final location: outside the cell, into the membrane, or to specific organelles. Sure! Here’s a simple explanation of that passage: In eukaryotic cells, ribosomes (which make proteins) come in two types based on where they are found: 1. Free ribosomes • These float in the cytoplasm by themselves or in clusters called polyribosomes. • They make proteins that stay inside the cell, especially in the cytosol (the fluid part of the cell). • Example: enzymes for glycolysis (the breakdown of glucose for energy). 2. Bound ribosomes • These are attached to the rough endoplasmic reticulum (RER). • They make proteins that will be modified, packaged, and either: • Sent to other organelles • Inserted into the cell membrane, or • Exported out of the cell
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Functions of the endomemmbrane system State the five components in animals. The protein in the smooth ER that keeps proteins there is called? What organelle is described as an extensive network of membranous tubules extending from the nuclear envelope to the plasma membrane? Note: smooth ER functions depends on where the cell is located. State some functions of the smooth ER(apart from drug detoxification, lipid synthesis and calcium ions storage) Proteins will only leave the RER only after proper folding has taken place. 4)Correctly folded proteins departs from the ER in vesicles that bud from a specialized region called transitional ER. 5)RER is also a membrane factory for the cell by producing transmembrane proteins for incorporation into ER itself or membranes of other organelles. Rough ER gives proteins their tags so they don’t leave, it fold them and gives them localization or signal destination to go to the golgi If the proteins don’t have these, the Golgi won’t accept them. Here are some MCQs based on the information you provided: 1. Why is the Rough Endoplasmic Reticulum (RER) studded with ribosomes? A. To aid in lipid synthesis B. To produce carbohydrates C. To facilitate protein synthesis and modification D. To store calcium ions Answer: C. To facilitate protein synthesis and modification Explanation: The ribosomes on the RER are involved in synthesizing proteins, particularly water-soluble and transmembrane proteins, which are then modified in the RER. 2. Which of the following is a function of the RER in pancreatic cells? A. Breakdown of old organelles B. Synthesis and secretion of insulin C. Storage of glycogen D. Filtration of waste products Answer: B. Synthesis and secretion of insulin Explanation: Pancreatic cells use their RER to synthesize and secrete insulin and digestive enzymes. 3. During protein synthesis, how does the RER contribute to glycoprotein formation? A. By phosphorylating proteins B. By attaching lipids to proteins C. By covalently attaching carbohydrates D. By removing amino acids Answer: C. By covalently attaching carbohydrates Explanation: As proteins enter the lumen of the RER, it adds carbohydrate groups to form glycoproteins. 4. What directs a newly synthesized protein into the lumen of the RER? A. A nuclear localization signal B. A carbohydrate chain C. An exit signal D. A pore in the RER membrane Answer: D. A pore in the RER membrane Explanation: Proteins being synthesized on the RER are guided through a pore into the RER lumen for modification. Let me know if you want these MCQs in a printable format or added to a quiz!
The endomembrane system are a group of organelles in eukaryotes that are normally connected physically and work together to post-process, modify, package and transport proteins and lipids. b.This system consists of the nuclear envelope, the endoplasmic reticulum, the golgi apparatus, lysosomes, peroxisomes and vacuoles (plants). The protein that keeps other proteins in the smooth ER (and also in the rough ER and ER lumen in general) is called the KDEL receptor. It recognizes a specific amino acid sequence at the C-terminus of proteins: KDEL = Lys-Asp-Glu-Leu How it works: • Proteins that are supposed to stay in the ER (like chaperones and folding enzymes) have the KDEL sequence. • If they escape to the Golgi by mistake, the KDEL receptor in the Golgi binds them and retrieves them back to the ER via vesicles. So, while KDEL is the sequence, the KDEL receptor is the protein responsible for retaining/retrieving ER-resident proteins. Endoplasmic reticulum (little net within the cytoplasm) An extensive network of membranous tubules extending from the nuclear envelope to the plasma membranes. It constitutes more than half of the total membrane of an average animal. The network of membranous tubules and sacs are called cisternae and the single internal space it surrounds is the ER cisternae space. It consists of smooth endoplasmic reticulum (SER) and the rough endoplasmic reticulum (RER). Functions of SER: oIn the liver, the SER that contain cytochrome P450 oxidative enzymes are involved in the detoxification of drugs, chemicals and poisons. oOther SER has the enzymes needed for the synthesis and metabolism of lipids including phospholipids, cholesterol and steroid hormones required for the production of new cell membranes. oSER are also responsible for production of lipoprotein. These are proteins that carry lipids in the bloodstream to other parts of the body. oSER also forms vesicles of large molecules which are transported to other parts of the cell e.g. the plasma membrane or Golgi apparatus. oSER stores calcium ions in muscle cells and upon stimulation by a nerve impulse, the calcium ions move into the cytosol to trigger a contractio
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Golgi is the major site for polysaccharide synthesis. Only proteins properly folded and assembled are allowed to leave the ER to the golgi. If not, their exit signals are removed and they’re destroyed in the ER. 1. What is the Golgi apparatus composed of? A. Flat sheets of rough ER B. A stack of 3-20 curved saccules C. A group of vesicles and ribosomes D. Several nucleoli and mitochondria 2. What is the function of the cis face of the Golgi apparatus? A. It directs vesicles toward the nucleus B. It secretes vesicles to the plasma membrane C. It receives vesicles from the ER D. It modifies DNA 3. The trans face of the Golgi apparatus is responsible for: A. DNA replication B. Receiving ribosomes C. Modifying proteins inside the nucleus D. Shipping mature vesicles to other locations 4. In the Golgi, where do budding vesicles from the ER empty their contents? A. Directly into the cytoplasm B. Into the mitochondria C. At the trans face D. At the cis face The golgi produced what two organelles? As the proteins move through the Golgi, they are modified, sorted, processed, packaged, warehoused and shipped for use in the cell or for distribution to other areas in the cell. Initial modification initially removes the glyco-tag received in the ER. 6.The Golgi also manufactures certain macromolecules by itself including lysosomes and peroxisomes for secretio
Lysosomes and peroxisomes for secretion. 1. Correct Answer: B. A stack of 3–20 curved saccules Explanation: The Golgi apparatus is made of a series of flattened, curved membrane-bound sacs called saccules. 2. Correct Answer: C. It receives vesicles from the ER Explanation: The cis face is oriented toward the ER and functions as the receiving end of the Golgi apparatus. 3. Correct Answer: D. Shipping mature vesicles to other locations Explanation: The trans face is the “shipping” side of the Golgi where fully processed proteins and lipids are sent to their final destinations. 4. Correct Answer: D. At the cis face Explanation: Vesicles from the ER fuse with the cis face of the Golgi and deliver their contents for further modification. Why doesn’t the vesicle go straight to the trans face? The Golgi apparatus functions as a processing center. The cis face is the “entry” point where proteins and lipids arrive from the ER. They then move through the saccules, getting chemically modified (e.g., glycosylation, tagging) as they pass from cis to medial to trans compartments. The trans face is the “exit” point that sorts and sends these mature products to their final destinations (like the plasma membrane or lysosomes).
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What compounds do lysosomes eliminate? What medium do lysosomes work best in? Acidic or basic? What internal ph do they have? What’s the ph of the cytoplasm and ph of the golgi? Why is it important that the ph of the cytoplasm is different from that of the lysosomes? State two ways lysosomes do their work. Genetic defects in lysosomal enzymes or receptors lead to accumulation of unwanted material that can inhibit normal cellular function. 1. accumulation of partially digested gangliosides that impairs brain function occurs in what genetic disease? 2. accumulation of glycogen particles – due to absence or deficiency of specific lysosomal enzymes. Note: Gaucher's disease or Gaucher disease is a genetic disorder in which glucocerebroside accumulates in cells and certain organs.
Lysosomes - digestive compartments A lysosome is a membranous sac of about 40 different hydrolytic enzymes (acid hydrolases) including proteases, nucleases, lipases, glycosidases, phosphatases etc. that are used to digest and eliminate unwanted material and recycling wanted components. The compounds eliminated are foreign particles, dead or injured tissues and the cell's own worn out organelles (autophagy). Lysosomes work best in an acidic medium and have an internal pH of 5.5 where most of its enzymes have maximum activity. Since the pH of the cytoplasm is about 7.2(golgi is 7.4), enzymes that escape from the lysosomes are inactivated thus protecting cytoplasmic contents. However, an extensive leak could cell autodigestion. Lysosomes carry out their digestion (i) by phagocytosis (engulfing smaller organisms) e.g. macrophages of white blood cells engulfing and destroying bacteria and ii) autophagy to recycle their own damaged or worn out material Genetic defects in lysosomal enzymes or receptors lead to accumulation of unwanted material that can inhibit normal cellular function. Examples are Tay-Sachs disease - accumulation of partially digested gangliosides that impairs brain function Pompe's disease - accumulation of glycogen particles - due to absence or deficiency of specific lysosomal enzymes.
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How do peroxisomes acquire their proteins? What enzymes do they contain? They are also abundant in cells that metabolize lipids - breaking down very long fatty acids to shorter chain fatty acids and finally to Acetyl CoA for fuel. •They also oxidize the side chain of cholesterol needed for bile synthesis and phospholipids for nerve cell myelination. Mutations affecting synthesis of functional peroxisomal enzymes or their import and incorporation into vesicles results in diseases. e.g. Zellweger’s syndrome is caused by absence of functional peroxisomes and death occurring by 6 months Explain what happens in zellwegers syndrome Note: hydrogen and oxygen to water is seen in the forming of ATp but as you grow older, instead of water, you form hydrogen peroxide so peroxisomes make sure everything is removed People with Zellweger disease will have an accumulation of very long-chain fatty acids (VLCFAs). Why? Zellweger syndrome is caused by a defect in peroxisome biogenesis. Peroxisomes are essential for breaking down very long-chain fatty acids (VLCFAs) through beta-oxidation. When peroxisomes are non-functional or absent: • VLCFAs cannot be broken down. • So, they accumulate in tissues like the brain, liver, and kidneys. • This buildup contributes to severe developmental issues and organ dysfunction. In contrast: Short-chain and medium-chain fatty acids are mainly broken down by mitochondria, not peroxisomes, so their metabolism is not directly affected in Zellweger syndrome. Let me know if you’d like a simple MCQ to test this concept!
Peroxisomes are membrane-bounded vesicles that do not contain DNA or ribosomes and thus acquire their proteins from selective import from the cytosol. They contain specific oxidative enzymes such as catalase that use molecular oxygen to remove hydrogen atoms in specific oxidative reactions that end up producing hydrogen peroxide. Catalase then uses the H2O2 to oxidise other substrates e.g. in the liver and kidney cells, the H2O2 are used to detoxify phenols and alcohols to produce water and oxygen. Let’s break it down simply: Peroxisomes are small organelles in your cells that help break down: • Fatty acids, especially very long-chain ones • Toxins like hydrogen peroxide (H₂O₂) To work, they need special enzymes inside them. Zellweger Syndrome: • This disease is caused by mutations in genes that are supposed to make these enzymes or help them get imported into peroxisomes. • Without these enzymes, peroxisomes can’t function. • In fact, in Zellweger’s, peroxisomes are basically non-functional or even absent. What happens in the body? • Fatty acids build up to toxic levels. • The brain, liver, and kidneys especially get damaged. • It leads to severe developmental issues. • Sadly, it is usually fatal within the first year, often around 6 months. In short: Zellweger syndrome is like a factory missing all its workers (enzymes), so nothing gets done, and toxic waste piles up — harming the whole body. Great question! In Zellweger syndrome, the enzymes themselves might not actually be missing — instead, they can’t get into the peroxisomes because of a defect in the import system. But if you’re asking about which enzymes are supposed to be in the peroxisomes, here are the key ones that are affected or fail to function properly: Key Enzymes Normally Found in Peroxisomes (and affected in Zellweger): 1. Acyl-CoA oxidase • Breaks down very long-chain fatty acids (VLCFAs). • Without it, VLCFAs build up in tissues (especially brain and liver). 2. Catalase • Breaks down hydrogen peroxide (H₂O₂) into water and oxygen. • Protects the cell from oxidative damage. 3. D-amino acid oxidase • Breaks down D-amino acids. 4. Urate oxidase (in some species) • Helps in purine metabolism (humans don’t really have this active form, but it’s relevant in other peroxisomal disorders). 5. Plasmalogen-synthesizing enzymes • Important for making plasmalogens, which are critical phospholipids in the brain and heart. Why They’re Missing or Nonfunctional in Zellweger: • Mutations often affect PEX genes (e.g., PEX1, PEX2, etc.). • These genes make proteins that help enzymes get into peroxisomes. • So, the enzymes might be made, but they’re floating uselessly in the cytoplasm, not inside the peroxisome where they’re needed. Summary: The main problem isn’t always the enzyme itself but the defective import system. Still, the end result is the same: peroxisomal enzymes don’t work, leading to toxic buildup and severe developmental issues.
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Relationships between the endomembrane organelles 1 Nuclear envelope is connected to rough ER(they’re close by each other), which is also continuous with smooth ER. 2 Membranes and proteins produced by the ck tlow in the form of transport vesicles to the Golgi. cis Golgi 3 Golgi pinches off transport vesides and other Vesides that give rise to lysosomes, other types of specialized vesicles, and vacuoles. Plasma 4 Lysosome is available for fusion with another vesicle for digestion. trans Jole § Transport vesicle carries proteins to plasma membrane for secretion. 6 Plasma membrane expands by fusion of vesicles; proteins are secreted from cell.. Most of the enzymes for cellular respiration are located in which part of the mitochondria? Which part of the mitochondria form the cristae? All eukaryotic cells have one or more mitochondria Mitochondria is to animals cells as what is to plant cells? Mitochondria can produce or has jrs own DNA(mother’s cytoplasm covers the nucleus of the sperm so mitochondria dna can be different from nuclear DNA.
Mitochondria and chloroplasts 1.Organisms need to transform external energy sources into usable energy and the mitochondria are responsible for this conversion. 2.Mitochondria are the sites for cellular respiration, the metabolic process that generates ATP by extracting energy from sugars, fats and other fuels with the help of oxygen. Most of the enzymes are in the matrix within the inner membrane. 3.Mitochondria has two membranes - inner and outer. The inner membrane forms the cristae which provides a much greater surface area for the complexes involved in cellular respiration. 4.The cristae project into the matrix, the inner space filled with semifluid medium containing enzymes involved in ATP production. 5.Mitochondria also contains small amounts of DNA that directs synthesis of proteins by its own ribosomes. All eukaryotic cells have one or more mitochondria. 6.Mitochondria is to animal cells as chloroplast is to plant cells. Sure! Here’s a simple explanation: Mitochondria and Their DNA: Mitochondria have their own DNA (called mtDNA), which comes only from the mother. This DNA makes proteins that are critical for the mitochondria to do their main job — producing energy (ATP) for the cell through aerobic respiration. Why Mutations in mtDNA Cause Disease: When mutations happen in mtDNA: • The mitochondria can’t make enough energy. • This mainly affects high-energy-demand tissues like: • Eyes (causing sudden blindness), • Muscles (leading to weakness), • Brain and nerves (causing neurological issues). Examples of Mitochondrial Diseases: 1. Leber’s Hereditary Optic Neuropathy (LHON) • Sudden vision loss in young adults (usually males). • Caused by mutations in mtDNA affecting optic nerve cells. 2. MELAS (Mitochondrial Encephalomyopathy, Lactic Acidosis, and Stroke-like episodes) • Affects the brain and muscles. • Causes seizures, headaches, and muscle fatigue. 3. Myoclonic Epilepsy with Ragged Red Fibers (MERRF) • Causes muscle jerks, seizures, and coordination issues. Mitochondria and Brain Disorders: • In disorders like Parkinson’s, Alzheimer’s, bipolar disorder, and schizophrenia, scientists have found: • Abnormal mitochondria or • Reduced energy production in brain cells. • The brain is very energy-hungry, so when mitochondria fail, brain function suffers. Summary: Mutations in mitochondrial DNA interfere with energy production, especially in organs like the brain, eyes, and muscles. That’s why mitochondrial diseases often cause blindness, muscle weakness, and neurological or mental health problems. Mitochondria help in making and recycling neurotransmitters • If energy is low: • Dopamine is affected → Parkinson’s • Serotonin and norepinephrine may be imbalanced → bipolar disorder and depression c. Cell Damage and Death • Without enough energy, brain cells: • Can’t repair themselves • Become stressed and die (called neurodegeneration) • This contributes to memory loss, movement issues, and mood disorders 3. Oxidative Stress and Toxins • Damaged mitochondria release free radicals (harmful molecules) • This causes oxidative stress, which damages more brain cells • It’s like a cycle that worsens brain function over time
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Which is a true statement about ribosomes? A.Ribosomes contain DNA and protein. B.Ribosomal subunits leave the nucleus after being formed by the nucleolus. C.Polyribosomes are the subunits of ribosomes. D.Ribosomes are only found associated with the endoplasmic reticulum in prokaryotic cells.   Which is NOT true of eukaryotic cells?   A.A true nucleus contains the chromosomes. B.Eukaryotic cells contain membrane-bounded compartments. C.They contain ribosomes that are smaller than those of prokaryotic cells. D.They contain many organelles in the cytoplasm. ●The cytoskeleton is a network of interconnected filaments and tubules that extends from the nucleus to the plasma membrane. ●Thus, organelles of an eukaryotic cell do not float freely in the cytoplasm but are organized due to its being held by these filaments throughout the cytoplasm. ●The cytoskeleton principally includes three types of molecular structures - actin filaments, intermediate filaments and microtubules. ●The function of the cytoskeleton is to give mechanical support to the cell and maintain the geometry of the cell shape. ●It also fixes the positions of the organelles and moves the compounds within the cell. ●The cytoskeleton is dynamic because they undergo rapid assembly and disassembly e.g. the formation of a spindle during cell division. Cytosol is the fluid between the cell membrane and the nucleus also known as the organelle free cell fluid. Many of the cells reactions occur in the cytosol including protein and fatty acid synthesis, metabolic reactions and pathways amongst others. Centrioles are short cylinders with nine sets of triplets. Cilia are shorter than flagella in eukaryotes. Nucleolus: Assembly of the subunits of ribosome for synthesis. RNA repair Centriole: Formation of basal bodies Cytoskeleton: Cell morphology, internal organization, motility and intracellular movements of parts Difference between prokaryotes and eukaryotes: Cytoplasmic membrane Cytoplasmic membrane without carbohydrates and usually lacking sterols. Incapable of endocytosis Cytoplasmic membrane contains sterols and carbohydrates and is capable of endocytosis (phagocytosis and pinocytosis) and exocytosi
Here are the correct answers with explanations: 1. Which is a true statement about ribosomes? Correct answer: B. Ribosomal subunits leave the nucleus after being formed by the nucleolus. Explanation: • A. Incorrect – Ribosomes contain RNA and protein, not DNA. • B. Correct – The nucleolus forms ribosomal subunits, which then exit the nucleus through nuclear pores to function in the cytoplasm or on the ER. • C. Incorrect – Polyribosomes are clusters of ribosomes translating the same mRNA, not subunits. • D. Incorrect – Ribosomes are found in both prokaryotes and eukaryotes, but not on the ER in prokaryotes (they lack ER). 2. Which is NOT true of eukaryotic cells? Correct answer: C. They contain ribosomes that are smaller than those of prokaryotic cells. Explanation: • A. True – Eukaryotes have a true nucleus with chromosomes. • B. True – Eukaryotic cells have membrane-bound organelles (e.g., ER, Golgi, mitochondria). • C. Not true – Eukaryotic ribosomes are larger (80S) compared to prokaryotic (70S). • D. True – Eukaryotic cytoplasm has many organelles.
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A short pygmy in Zaire, an overweight adult with diabetes and a child with high cholesterol in blood may have nothing in common or so you think. Each suffers from a defect in the cells of the plasma membrane. ➢The pygmy’s plasma membrane will not allow growth hormone to bind to receptors ➢The diabetic plasma membrane do not respond to insulin due to lac of or reduced insulin receptors ➢The young child’s plasma membrane prevent entry of lipoproteins which are cholesterol carriers In all these three cases, the plasma membrane is to be blamed. The fact that we are seeing three very different and independent conditions from the same source shows the diverse roles plasma cells play in our daily lives. The plasma membrane also has the ability to detect self from non-self and is essential in transplant rejections. ➢The side that faces the cytoplasm is the intracellular face and the side that faces outward is the extracellular face Chemical analysis showed that the amount of phospholipids present was twice as much was needed per surface area so a bilayer was proposed. Ampiphatic phospholipid has a polar head made of choline, phosphate and glycerol and the tail is made of fatty acids. Cholesterol molecules are found near the membrane surface. The phospholipids by flexing their tails can drift laterally from place to place and this movements provides the fluidity of the membrane By interacting with the phospholipids and holding them still, cholesterol can stiffen the membranes. So the cell membrane is made up of 70% phospholipids,25% cholesterol and 5% glycolipids(phospholipids with short carbohydrate chains on the extracellular face of the membrane.) oLipids alone could not account for permeability to non lipid (polar) substances suggesting that proteins must be a part of the plasma membrane. oProteins constitute about 5-10% of the molecules of the plasma membrane. However since they are larger than lipids, they constitute about 50% of the membrane weight. oThe plasma membrane therefore is seen as a thin film of majority lipid and minority protein molecules held together by noncovalent interactions. Membrane proteins Peripheral proteins do not protrude into the phospholipid layer and locate either on the outside or the inside surface of the membrane. Transmembrane/integral proteins pass through the membrane. They have their hydrophilic regions in contact with the cytoplasm and extracellular fluid i.e. projecting from both surfaces of the bilayer. The hydrophobic regions of the integral proteins are embedded within the membrane. Many of these proteins drift about freely in the phospholipid film whilst others are anchored to the cytoskeleton. Dynamic Fluid Mosiac model The hydrocarbon tails can wiggle and the entire phospholipid bilayer can move sideways creating the fluidity. This makes the cells pliable/flexible. The fluidity of the membrane is thus dependent on the lipid components and this is critical for proper functioning of the membrane proteins. The cell membranes is also dynamic so that most of the molecules including proteins are free to drift laterally in the plane of the membrane. each membrane has a their unique collection of the type of proteins. Myelin membrane which is used for insulation has about 25%of mass as protein whilst internal membranes of the mitochondria has about 75% protein. Membrane proteins just like membrane lipids have oligosaccharide chains attached to them that face the cell exterior. ➢Thus the surface of the cell presenting to the exterior is rich in glycoproteins such as lectins. This protects the cell surface from mechanical and chemical damage. ➢Despite the function of the protein, there are always many more lipid molecules than protein molecules in membranes (50:1
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State the six types of membrane proteins and state four functions of membrane proteins
Channel/carrier proteins – A protein that spans the membrane and may provide a hydrophilic channel across the membrane. Others transport by changing shape. Carrier proteins selectively interact with a specific molecule or ion in order to cross the membrane e.g. sodium-potassium pump. May or may not require ATP. ➢Cell recognition proteins - which are unique due to specific identification tags which are recognized by membrane proteins of other cells. ➢Intercellular joining proteins – Membrane proteins of adjacent cells may hook together in various kinds of junctions. ➢Receptor proteins/signal transduction – An external messenger (signaling molecule) binds to the receptor and causes a change in protein conformation that results in the relay of message into the cell. ➢Enzymatic proteins – This may have the active site exposed to substances in the solution or may be a group of enzymes that carry out sequential steps of a metabolic pathway. ➢Cytoskeletal attachment – Non-covalent binding with cytoskeletal filaments to maintain shape and location. Exactly! These are functions of membrane proteins, and each type has a distinct role in maintaining cell structure, communication, transport, and interaction. Here’s a quick breakdown: 1. Receptor proteins – Bind to signaling molecules (like hormones) and trigger a response inside the cell. 2. Enzyme proteins – Catalyze chemical reactions, such as breaking down messengers after their job is done. 3. Ion channel proteins – Provide always-open passageways for specific ions to cross the membrane. 4. Gated ion channels – Open or close in response to signals (voltage, chemicals, or pressure), regulating ion flow. 5. Cell-identity markers – Usually glycoproteins that let the immune system recognize the cell as self or foreign. 6. Cell-adhesion molecules (CAMs) – Help cells stick together and interact, crucial for tissue structure and repair. Would you like MCQs on this too?
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1. The glycocalyx is best defined as: A. A lipid bilayer embedded with proteins B. The carbohydrate-rich coating on the outer surface of the cell membrane C. A fibrous protein network on the inside of the nucleus D. The inner mitochondrial membrane involved in ATP synthesis 2. Which component is responsible for the formation of the glycocalyx? A. Ribosomes and mRNA B. Phospholipids and cholesterol C. Glycolipids and glycoproteins D. Actin and myosin 3. Which of the following statements is TRUE about the glycocalyx? A. It is the same in all humans B. It helps in ATP generation C. It guides immune cells in identifying self from non-self D. It is present inside the cytoplasm 4. The glycocalyx plays an important role in all the following EXCEPT: A. Transplant compatibility B. Immunity against infections C. Fertilization D. DNA replication 5. What makes the glycocalyx a target for immune attack in cancer cells? A. Its ability to produce hormones B. Its genetic material C. Changes in the glycoprotein patterns on its surface D. Presence of lysosomal enzymes 6. How does the glycocalyx contribute to embryonic development? A. It forms the neural tube B. It helps embryonic cells migrate to their correct location C. It differentiates organs D. It releases hormones to stimulate growth 7. The glycocalyx contributes to cell adhesion by: A. Producing antibodies B. Binding to the cytoskeleton only C. Helping cells stick together via surface recognition D. Fusing cells permanently 8. Which of the following diseases may result from dysfunction or absence of glycocalyx? A. Heart failure B. Autoimmune disorders C. Diabetes insipidus D. Scurvy 9. How does the glycocalyx contribute to protection of the plasma membrane? A. By forming lipid rafts that repel foreign bodies B. By producing antibodies C. By cushioning the membrane from mechanical and chemical damage D. By increasing DNA replication efficiency 10. In terms of organ transplants, what role does the glycocalyx play? A. It stimulates antibody production in the donor B. It determines tissue compatibility through unique cell surface markers C. It repairs damaged tissue after transplant D. It triggers organ growth in the recipient 11. During fertilization, how does the glycocalyx aid sperm recognition? A. It changes the shape of the egg B. It secretes enzymes to guide the sperm C. It displays specific carbohydrate markers that sperm can recognize D. It fuses with the sperm’s tail to pull it in 12. Why is the glycocalyx important in preventing auto-destruction of the body’s own cells? A. It removes harmful DNA from the cytoplasm B. It absorbs excess hormones C. It acts as an identity tag distinguishing self from foreign D. It increases metabolic activity MCQs – Disorders Related to the Plasma Membrane 1. Which of the following best explains how Clostridium perfringens contributes to gas gangrene? A. It blocks sodium channels on neurons B. It releases a lipase that destroys phospholipids and sphingomyelin C. It creates pores for bacteria to enter cells D. It overactivates chloride channels in intestinal cells 2. How does the cholera toxin affect intestinal cells? A. It causes glucose to leak into the bloodstream B. It blocks all forms of ion transport C. It interferes with adenylate cyclase and causes ion and water loss D. It increases protein synthesis in epithelial cells 3. Why does cholera lead to dehydration? A. It reduces water absorption in the colon B. It causes chloride and sodium to enter cells C. It causes sodium and chloride to leave cells, pulling water with them D. It blocks aquaporins from working 4. What effect does chronic alcoholism have on the plasma membrane? A. It causes complete membrane breakdown B. It makes the membrane more rigid, affecting blood flow C. It increases membrane fluidity and disrupts neurotransmission D. It permanently blocks ion channels 5. In cystic fibrosis, what is faulty in the plasma membrane? A. Sodium pump B. Glucose transporter C. Chloride channel D. Cholesterol content 6. What effect does the faulty chloride channel in cystic fibrosis have? A. Causes loss of glucose through the skin B. Results in thick mucus in airways and pancreas C. Increases water absorption in the lungs D. Enhances resistance to dehydration 7. Why are pygmies naturally shorter than average? A. They lack growth hormone B. Their plasma membranes don’t produce insulin C. They have defective growth hormone receptors in the plasma membrane D. Their bones lack calcium receptors
Answers and Explanations 1. B. The carbohydrate-rich coating on the outer surface of the cell membrane The glycocalyx is a fuzzy, sugary coating made from glycoproteins and glycolipids extending from the plasma membrane. 2. C. Glycolipids and glycoproteins These are the key components that extend their carbohydrate chains into the extracellular space to form the glycocalyx. 3. C. It guides immune cells in identifying self from non-self Each person’s glycocalyx is unique (except identical twins), enabling immune cells to distinguish between self and foreign cells. 4. D. DNA replication DNA replication occurs in the nucleus and is not related to the glycocalyx. 5. C. Changes in the glycoprotein patterns on its surface Cancer cells often modify their surface glycoproteins, making them recognizable as foreign by the immune system. 6. B. It helps embryonic cells migrate to their correct location The glycocalyx helps guide cells during embryonic development to ensure proper tissue and organ formation. 9. C. By cushioning the membrane from mechanical and chemical damage The glycocalyx acts as a protective coat, reducing physical stress and preventing chemical injury. 10. B. It determines tissue compatibility through unique cell surface markers Because each person’s glycocalyx is different, it influences whether the body accepts or rejects transplants. 11. C. It displays specific carbohydrate markers that sperm can recognize These markers help sperm identify and bind to the correct egg species. 12. C. It acts as an identity tag distinguishing self from foreign This prevents the immune system from attacking the body’s own healthy cells. 7. C. Helping cells stick together via surface recognition The glycocalyx enables cells to adhere to one another, maintaining tissue structure. 8. B. Autoimmune disorders If the immune system fails to properly recognize the body’s own glycocalyx, it can trigger autoimmune responses Answers & Explanations 1. B – The bacteria secrete a lipase that breaks down key membrane lipids, disrupting normal cell function. 2. C – The AB-toxin disrupts adenylate cyclase function, causing ionic imbalance and water loss. 3. C – The exit of Na⁺ and Cl⁻ into the lumen draws water out osmotically, leading to severe dehydration. 4. C – Ethanol inserts itself into the membrane, increasing fluidity, which impairs ion channels and slows neurotransmission. 5. C – The chloride channel is defective in cystic fibrosis. 6. B – The faulty channel causes thick mucus to accumulate in the airways and pancreas. 7. C – Pygmies have faulty growth receptors on their plasma membranes, leading to short statur Diseases and disorders associated with the plasma membrane One bacteria toxin secreted by Clostriduim perfringens (gas gangrene) is a lipase that hydrolyzes phospholipids and sphingomyelin and disrupts normal cell functioning. The AB-toxin of cholera interferes with proper functioning of adenylate cyclase, breaching the plasma membrane of certain channels. Sodium and chloride ions leave the intestinal cell into the lumen and water follows causing severe dehydration. Excessive alcoholism causes an increase in membrane fluidity due to the intercalation of ethanol between membrane lipids. This affects ion channels for neurotransmitters, slowing down nervous transmission. Cystic fibrosis has a faulty chloride channel on the plasma membrane, resulting in thick mucous collection in airways and pancreatic ducts. Pygmies are short because their plasma membrane growth receptors are faulty. Non
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Great observation — yes, gluconeogenesis does partly occur in the mitochondria, though most of it happens in the cytoplasm. Here’s a breakdown: Where Gluconeogenesis Happens: 1. Mitochondria: • The first step of gluconeogenesis occurs here. • Pyruvate → Oxaloacetate (enzyme: pyruvate carboxylase) • This step requires biotin and occurs only in the mitochondrial matrix. • Oxaloacetate is then converted to malate or aspartate to leave the mitochondria. 2. Cytoplasm: • Once outside the mitochondria, malate/aspartate is converted back to oxaloacetate. • Gluconeogenesis continues: • Oxaloacetate → Phosphoenolpyruvate (PEP) (enzyme: PEP carboxykinase) • Followed by a series of steps that ultimately form glucose. Summary Table: Step Location Enzyme Pyruvate → Oxaloacetate Mitochondria Pyruvate carboxylase Oxaloacetate → PEP Cytoplasm PEP carboxykinase Later steps to glucose Cytoplasm Various enzymes So yes — mitochondria are involved at the beginning of gluconeogenesis. The rest continues in the cytoplasm. Let me know if you want a visual flowchart! Glycolysis
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The plasma membrane is differentially permeable allowing some substances such as hydrocarbons, carbon dioxide and oxygen to cross it easily without any aid. ➢Non-charged lipid soluble compounds such as alcohol, glucose and other sugars can slip between and pass through very slowly. Macromolecules are too large to enter. Note that non charged doesn’t mean non polar. Just because something is non charged doesn’t mean it’s non polar. It could be polar but not charged. So these particular molecules that move slowly are lipid soluble but polar. If a molecule has only a little polarity or if it has both polar and nonpolar parts, it can still dissolve in lipids. Small polar molecules with nonpolar parts can be lipid-soluble. Examples: • Ethanol (alcohol) • Methanol • Acetone • Urea (a little bit, but very slow) • Small amines (like methylamine) Summary: • These molecules have polar groups (like –OH or =O), • but they are small and have nonpolar parts, • so they can dissolve in lipids and cross membranes easily or moderately. ➢Ions and other polar molecules which are hydrophilic cannot enter the hydrophobic bilayer. ➢A polar molecule such as water may follow their concentration gradient to cross the membrane but that is not easy. ➢Since polar compounds also transverse the membrane, then special means must be used to get most substrates across the Membrane Cholera toxin forces the cells in the intestines to push out too much salt (sodium and chloride) into the gut. Because there’s now so much salt in the gut, water follows the salt by simple diffusion into the gut to balance it out. This causes lots of water loss from the body, leading to severe dehydration and low blood volume (hypovolemic shock). The water moves from inside the body (the intestinal cells and blood vessels) → into the gut (the lumen of the intestine). State the factors affecting rate of diffusion
Factors affecting rate of diffusion Membrane permeability – diffusion depends on how permeable a membrane is to the particles. Non-polar hydrophobic lipid-soluble substances diffuses easily through the phospholipid regions of the plasma membrane. Membrane surface area – by having villi in the small intestines there is increase membrane surface for diffusion and absorption. Temperature – The warmer a substance is the more rapidly its particles diffuse- sugar in warm tea diffuses quicker than iced tea. This is due to the kinetic energy of the particles. Molecular weight – heavy molecules such as proteins move more sluggishly and diffuse more slowly than light particles such as gases. Concentration difference – particle diffuse more rapidly is there is a greater concentration difference e.g. using an oxygen mask increases the rate of oxygen diffusion into a patient’s blood.
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Here are MCQs from your text: 1. What is osmosis? A) Movement of solute from high to low concentration B) Movement of solvent from low solute concentration to high solute concentration C) Movement of solute from low to high concentration D) Movement of solvent from high solute concentration to low solute concentration 2. What drives osmosis? A) Energy input from the cell B) Random movement of solute particles C) Difference in solute concentrations D) Active transport mechanisms 3. Through what does osmosis occur? A) A fully permeable membrane B) A semi-permeable membrane C) A waterproof membrane D) A rigid wall 4. Which statement about a semi-permeable membrane in osmosis is true? A) It allows both solute and solvent to pass. B) It only allows solute to pass. C) It only allows solvent (like water) to pass. D) It blocks both solute and solvent. 5. What happens when osmosis continues? A) The concentration difference increases. B) Both sides reach isotonicity (equal concentration). C) The solvent moves back and forth with no effect. D) Solute concentration becomes zero on both sides. You’re correct that diffusion itself doesn’t require energy. Here’s how it works: • Channel proteins: They are like specific gates in the membrane. They allow only certain molecules or ions to pass through, based on their size(bigger the size and the more the charge, the harder the diffusion so they’ll need carrier or channel proteins. The smaller the molecule or the more neutral or non charged the molecule, the easier it is)or charge. Since this movement follows the concentration gradient (from high to low concentration), it doesn’t require energy — this is a form of passive transport. • Carrier proteins: These proteins work by changing shape to move the molecule across the membrane. The molecule binds to the carrier protein on one side, and then the protein changes shape to release it on the other side. This process can also occur without energy if it’s moving down the concentration gradient (like simple diffusion). However, if the molecule needs to move against its concentration gradient (from low to high concentration), energy is required. This is known as active transport, and it uses ATP (the body’s energy currency) to “pump” the molecule across the membrane. So, if the molecule is moving down the gradient (high to low), no energy is needed (passive transport). But if it’s moving up the gradient (low to high), energy is required (active transport).
Here are the answers only: 1. B) Movement of solvent from low solute concentration to high solute concentration 2. C) Difference in solute concentrations 3. B) A semi-permeable membrane 4. C) It only allows solvent (like water) to pass. 5. B) Both sides reach isotonicity (equal concentration). Let me know if you want a super quick summary too! Osmosis is the net movement of a solvent solution from a region of low solute concentration (hypotonic) to a region of high solute concentration(hypertonic) through a semi-permeable membrane in order to achieve isotonicity on both sides. Osmosis proceeds without the input of energy and the semi-permeable membrane is permeable only to the solvent and not the solute. M
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Here are the MCQs based on the text: 1. What facilitates the passage of glucose and amino acids across the plasma membrane? • a) Lipid solubility • b) Facilitated transport via carrier or channel proteins • c) Simple diffusion • d) Active transport via ATP 2. What is required for glucose and amino acids to pass through the membrane in facilitated transport? • a) Energy input (ATP) • b) Reversible combination with specific carrier proteins • c) Increase in temperature • d) Decreased concentration gradient 3. Which of the following cells do not have facilitative glucose transporters? • a) Red blood cells (RBCs) • b) Pancreatic cells • c) Liver cells • d) Brain cells • e) All cells except brain, RBCs, pancreas, and liver 4. What effect does insulin have on glucose transport? • a) Decreases glucose transport • b) Increases glucose transport • c) No effect on glucose transport • d) It prevents glucose transport 5. In individuals with diabetes who do not produce insulin, what happens to glucose transport? • a) It increases significantly • b) It decreases, leading to hyperglycemia • c) It remains unaffected • d) It causes the glucose to be absorbed into tissues at a faster rate 6. Facilitated transport of glucose occurs: • a) Against a concentration gradient using energy • b) Down a concentration gradient without the use of energy • c) By passive diffusion • d) Using protein pumps that require ATP Let me know if you’d like the answers to these!
Here are the answers to the MCQs: 1. What facilitates the passage of glucose and amino acids across the plasma membrane? • Answer: b) Facilitated transport via carrier or channel proteins 2. What is required for glucose and amino acids to pass through the membrane in facilitated transport? • Answer: b) Reversible combination with specific carrier proteins 3. Which of the following cells do not have facilitative glucose transporters? • Answer: e) All cells except brain, RBCs, pancreas, and liver 4. What effect does insulin have on glucose transport? • Answer: b) Increases glucose transport 5. In individuals with diabetes who do not produce insulin, what happens to glucose transport? • Answer: b) It decreases, leading to hyperglycemia 6. Facilitated transport of glucose occurs: • Answer: b) Down a concentration gradient without the use of energy Let me know if you need further clarifications! Glucose moves down the concentration gradient when entering cells because of facilitated diffusion. This process occurs when glucose is transported from an area of higher concentration (outside the cell) to an area of lower concentration (inside the cell), which is the natural direction of movement in diffusion. Even though glucose is not lipid-soluble and cannot directly pass through the membrane, it still follows the concentration gradient because the carrier proteins (like GLUT transporters) provide a pathway for glucose to move into the cell without using energy. The cells only need glucose when they require it for energy or other metabolic processes, so the concentration of glucose inside the cell tends to be lower than the concentration outside the cell, allowing glucose to move into the cell naturally. Here’s the difference simply: • Facilitated diffusion glucose (what we talked about before) moves alone using a carrier protein, from high to low concentration, no energy needed. Using GLUT • Sodium-glucose co-transport (SGLT) happens mainly in the intestine and kidney. Here, glucose moves together with sodium (Na⁺) into the cell. Even if glucose is low outside, it can still enter, because sodium’s strong gradient drags it in. Energy is indirectly used because sodium’s gradient is kept strong by the sodium-potassium pump (which uses ATP). In short: • Facilitated diffusion = glucose moves alone, high to low, no direct energy. • Sodium-glucose co-transport = glucose rides with sodium, can move even against its own gradient, needs energy indirectly. Here’s a simple list: • GLUT1 – Found in the brain, RBCs (red blood cells), and placenta (basically important for constant glucose supply). • GLUT2 – Found in the liver, pancreas (beta cells), kidneys, and small intestine (works when glucose is high; low affinity, high capacity). • GLUT3 – Found mainly in the neurons (very high affinity for glucose). • GLUT4 – Found in muscle and fat (adipose) tissue; insulin increases its activity. • GLUT5 – Mainly transports fructose (found in small intestine). Each GLUT is specialized based on the tissue’s needs! Want a quick trick to remember them too? Would you like a short MCQ to test it too? Facilitated transport (Transport of glucose) This explains rapid passage of glucose and amino acids across the plasma membrane even though they are not lipid soluble using carrier or channel proteins. Their passage is facilitated by their reversible combination with specific carrier proteins. Energy is not required for this mechanism of transport as they move down a concentration gradient. outside All cells except brain, RBCs, pancreas and liver have facilitative glucose transporters that transport glucose from plasma membrane into the cell. Insulin increases this facilitative transport. Diabetes patients who do not produce insulin have decreased ability to transport glucose, hence the hyperglycemia.
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In active transport, molecules or ions move through the plasma membrane accumulating on either part of the membrane. 2.In this case, molecules are moving from a region of lower concentration to a region of higher concentration, so energy must be used to concentrate or drive the compound to one side of the membrane. 3.Proteins involved in this movement are called pumps and one pump - the sodium-potassium pump moves three Na+ ions to the outside and two K+ inside the cell. This two events are linked. 4.A change in carrier shape after attachment and detachment allows it to combine alternatively with sodium and potassium ions. So carrier proteins are used in Active transport as well. Just that carrier proteins in active transport use energy but those in passive don’t use energy. Channel proteins aren’t used here though. Carrier proteins always change shape. • In facilitated diffusion → shape change happens without energy. • In active transport → shape change happens because ATP gives energy to force the movement. 5.For the exchange to be possible, ATP is consumed Note: Tetradotoxin from puffer fish (fugu-popular Japanese fish) bind to the voltage dependent Na+ channel protein in nerve cells and block the movement of Na+. Which can lead to paralysis cuz sodium isn’t entering to depolarize the cell so nerve signals aren’t being conducted. So this is a voltage gated channel. We also have leaky channels where anything passes anytime at all. Other toxins keep the channel permanently open example is Batrachotoxin: • Found in the skin of certain frogs (e.g., Phyllobates species). • Effect: Batrachotoxin prevents the closure of sodium channels, causing them to stay open. • Result: This leads to an excessive influx of sodium into cells, which causes continuous depolarization and can result in muscle spasms, seizures, and ultimately paralysis. It can lead to paralysis because If prolonged, the inability to relax muscles results in paralysis, as the muscle remains locked in a contracted state and cannot respond to new signals.
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For membrane assisted transport specifically bulk flow, Macromolecules such as polypeptides, polysaccharides are too large to be transported by carrier proteins. They are transported in and out of cells by vesicle formation. During exocytosis, vesicles carrying a specific molecule fuse with the plasma membrane and its contents are exuded/secreted from the cell During endocytosis, cells take in substances by vesicle formation. A portion of the plasma membrane envelopes the substance and then pinches off to form the intracellular vesicle. When the material taken in is large such as a food particle or another cell, the process is called phagocytosis e.g. macrophages engulfing bacteria or RBC in mammals. When the vesicle forms around liquid or very small particles, the process is called pinocytosis. Blood cells, kidney cells use this method to ingest solutes. Receptor mediated endocytosis: Here’s a simple explanation of what your text is saying: Receptor-mediated endocytosis This enables cells to acquire bulk quantities of specific substances such as vitamins, hormones and lipoproteins even if they are not concentrated in the extracellular fluid. These serve as ligands. Embedded in the membranes are proteins with specific receptor sites which can bind to its corresponding ligand. The presence of the ligand causes these receptor proteins to gather at one location called coated pit where binding between ligand and receptor takes place. Receptor-mediated endocytosis is a special way cells pick up specific substances from outside, even if those substances are in very small amounts. • The cell has special receptors (like “locks”) on its membrane that can recognize and bind certain molecules (called ligands, e.g., vitamins, hormones, LDL). • When the ligand binds to its receptor, the receptors gather together at one spot on the membrane, called a coated pit. • The membrane then folds inward and forms a vesicle (a small bubble) that brings the ligand inside the cell. • Inside the cell, depending on what is inside: • Some substances are released for the cell to use. • Some are broken down by lysosomes (the “digestion centers” of the cell). • After unloading, the vesicle joins back with the membrane and the process can start again. Familial hypercholesterolemia example: • Normally, LDL (bad cholesterol) binds to LDL receptors on cells and is taken into the cell. • In people with this disease, the receptors don’t work properly or are fewer in number. • So, cholesterol stays in the blood instead of entering cells. • This causes buildup in blood vessels, leading to high blood pressure and heart attacks. Good — let’s go slowly, step-by-step: Your text said: “Once done, the membrane vesicle fuses with the plasma membrane to restart the process.” What it means is this: • After the vesicle enters the cell and delivers its cargo (the ligands like LDL, vitamins, etc.), • The vesicle membrane (especially the parts carrying the receptors) can move back and fuse with the plasma membrane. • Not the whole vesicle with the cargo — the membrane and receptors are recycled and rejoin the plasma membrane. • This is to restart the process — so the cell doesn’t waste receptors and can keep capturing new ligands. In very simple terms: • Vesicle enters → drops cargo → parts of vesicle (especially receptors) → go back → fuse with plasma membrane → ready to catch more ligands. Why is this important? Because if receptors were not recycled, the cell would quickly run out of receptors and stop functioning properly. Short simple version: After capturing substances, the vesicle sends its receptors and membrane parts back to the surface to catch more substances. Would you like a quick “story-style” example with LDL to make it even easier? (It might take just 5 lines!)
Note: vitamins, hormones and lipoproteins are examples of specific ligands. Conclusion: • In receptor-mediated endocytosis, the process happens when there are small amounts of specific ligands (like LDL) in the blood. • The presence of ligands causes the receptors on the membrane to gather together and form a coated pit. • Binding of the ligands to the receptors triggers vesicle formation. • The vesicle enters the cell. • Depending on the cargo, the contents are either digested by lysosomes or released into the cytoplasm. • The part of the vesicle that has the receptors returns and fuses with the plasma membrane. • This recycles the receptors, keeps their number high, and allows the cell to restart the process without wasting receptors. Tiny note: It doesn’t lead to exocytosis immediately after entry. Exocytosis is a different action where vesicles release things out of the cell. In this receptor-mediated endocytosis case, after internal delivery and receptor recycling, the receptors just return — they don’t do exocytosis yet Clinical implication of the receptor mediated endocytosis Familial hypercholesterolemia (FH) In this genetic disorder, the total concentration of cholesterol and LDL in the blood plasma is markedly elevated. The molecular defect in FH is the absence or deficiency of functional receptors for LDL. These receptors are needed for intake of LDL into peripheral cells and into the liver via receptor mediated endocytosis Homozygotes have no functional receptors whilst heterozygotes have about half of the normal number. Thus blood cholesterol levels increases i.e. 680mg/dL and 300mg/dL respectively. A value of <200mg/dL is desirable. The high concentration of cholesterol results in its deposition in tissues as yellow nodules called xanthomas which become prominent in skin and tendons. Furthermore, the excess LDL is oxidized to oxLDL, whch is taken up by macrophages, become trapped in wall of blood vessels and contribute to atherosclerosis and heart attacks. Most homozygotes die of coronary artery disease in childhood and seldom survive their 30th birthday Homozygotes: A person who inherited two bad copies of the gene (one from each parent). → In FH, they have no functional LDL receptors at all. • Heterozygotes: A person who inherited only one bad copy and one normal copy of the gene. → In FH, they have about half the normal number of LDL receptors.
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Amino acids, sugars and ions move by active transport. Examples of substances that use exocytosis(focuses on vesicle fusing with membrane): (You are right — exocytosis is mainly used for macromolecules.) Examples: • Hormones (e.g., insulin) • Enzymes (e.g., digestive enzymes) • Neurotransmitters (e.g., acetylcholine) • Waste products (from cells) 3. Receptor-mediated endocytosis(vesicles are formed here): (Also mainly for macromolecules.) Examples: • LDL (cholesterol transporter) • Insulin • Growth factors • Iron bound to transferrin 4. Regular endocytosis(vesicles are formed here): • Phagocytosis (cell eating): big things like bacteria, dead cells, subcellular materials(remains of a cell or some parts of the cell like pieces of some organelles) • Pinocytosis (cell drinking): small droplets of fluid and dissolved molecules (nonspecific) Question 7 Which one of the following is not a function of membrane proteins? Membrane proteins: A.provide cellular identification tags. B.attach the membrane to the cytoskeleton. C.form junctions between cells. D.serve as enzyme receptors.
Saturation occurs when all available transport proteins (like carrier proteins) are fully occupied by molecules. • In Active Transport and Facilitated Diffusion: • When the carrier proteins or channels are fully occupied, increasing the concentration of the transported molecule won’t increase the transport rate. • Once the carriers are “saturated,” the system can no longer transport any more molecules, regardless of how many are available. • Example: If too much glucose is available for a limited number of GLUT transporters, the transport rate will level off. Question 7: Why Answer D for “Not a Function of Membrane Proteins”? Answer: D. Serve as enzyme receptors Explanation: • A. Provide cellular identification tags – Membrane proteins (especially glycoproteins) are involved in cellular recognition. • B. Attach the membrane to the cytoskeleton – Membrane proteins like integrins help link the membrane to the cytoskeleton. • C. Form junctions between cells – Proteins like cadherins and connexins are responsible for forming junctions between cells. • D. Serve as enzyme receptors – This option is misleading. While membrane proteins can act as receptors for signals (like neurotransmitters or hormones), enzymes themselves are not typically receptors. Enzyme activity in the membrane is not commonly referred to as “receptors.” Therefore, D is not as fitting as the others, making it the least accurate choice here.
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A