cell cycle checkpoints and apoptosis

Question 1

What is the primary purpose of the cell cycle?

Answer 1

To produce two identical daughter cells

The cell cycle consists of a series of events ensuring accurate genome replication and distribution.

Question 2

What are the three main checkpoints in the cell cycle?

Answer 2

G1, G2, M

These checkpoints ensure the integrity of the DNA and proper cell division.

Question 3

What happens at the G1 checkpoint?

Answer 3

The DNA is checked for damage or incompleteness
* if the cell akes it through it can pass onto the S phase

If issues are found, the cell may enter the G0 stage or be targeted for destruction. this check is performed by a protein that is known as a tumour suppressor proteins.

Question 4

What role does the protein p53 play in the cell cycle?

Answer 4

It acts as a ‘security guard’ at the G1 checkpoint

Mutations in the p53 gene can lead to uncontrolled cell division.

Question 5

What is checked during the G2 checkpoint?

Answer 5

the cell now has double the amount of DNA after S-phase
The completeness and lack of damage of the replicated DNA

Passing this checkpoint allows the cell to advance to mitosis.

Question 6

What is the function of the M checkpoint?

Answer 6

To ensure sister chromatids are correctly attached to the spindle
if an error is detected the cell cycle is delayed until the problem is fixed. (it checks if the chromosomes can align well in metaphase and replicate/split evenly.)

Delays the cell cycle if errors are detected.

Question 7

What are spindle fibres and their role in mitosis?

Answer 7

Microtubule clusters that anchor chromosomes during metaphase

They are essential for the proper segregation of chromosomes.

Question 8

What is a kinetochore?

Answer 8

A protein complex that binds chromosomes to spindle microtubules

This attachment is crucial for chromosome movement during mitosis.

Question 9

What are proto-oncogenes?

Answer 9

Genes that produce proteins to initiate the cell cycle

Mutations can convert them into oncogenes, leading to cancer.

Question 10

What is the role of tumor-suppressor genes?

Answer 10

To signal the cell to reduce division, repair DNA, or initiate programmed cell death

Mutations in these genes can also lead to cancer.

Question 11

What organelles replicate during the cell cycle?

Answer 11

Mitochondria and chloroplasts

Their replication is essential to maintain cell function and structure.

Question 12

What is meristematic tissue in plants?

Answer 12

Tissue that can divide to produce identical daughter cells

Found in root tips and stems, it is crucial for plant growth.

Question 13

What process plays a crucial role in the reproduction of fungi?

Answer 13

The cell cycle

It enables fungi to grow and reproduce effectively.

Question 14

What is apoptosis?

Answer 14

Programmed cell death that is genetically controlled and highly regulated.

Question 15

What is the relationship between cell production and cell death in adults?

Answer 15

The rate of cell renewal equals the rate of cell death.

Question 16

What triggers apoptosis in cells?

Answer 16

Damage to the cell’s DNA detected by the organism.

Question 17

List some types of cells that undergo apoptosis.

Answer 17

• Cells at the end of their natural life
• Dysfunctional, damaged, or diseased cells
• Excessive cells

Question 18

What are the two mechanisms of apoptosis?

Answer 18

• Intrinsic (internal) signal pathway
• Extrinsic (external) signal pathway

Question 19

What happens to a cell during apoptosis?

Answer 19

• Cell shrinkage
• Formation of blebs
• Formation of apoptotic bodies

Question 20

What is the role of the protein p53 in apoptosis?

Answer 20

It leads to leakage of cytochrome c from the mitochondria, activating the apoptosome.

Question 21

What is the role of caspases in apoptosis?

Answer 21

They are proteins that break down proteins within the cell, leading to cell breakdown.

Question 22

What is a characteristic of cancerous cells compared to normal cells?

Answer 22

Cancerous cells divide in an unregulated manner and do not exhibit contact inhibition.

Question 23

What are proto-oncogenes?

Answer 23

Genes that signal cells to continue dividing.

Question 24

What are tumor-suppressor genes?

Answer 24

Genes that signal cells to stop dividing.

Question 25

What is the term for mutated proto-oncogenes that lead to cancer?

Answer 25

Oncogenes.

Question 26

What is metastasis?

Answer 26

The process by which cancer cells spread to other parts of the body.

Question 27

Fill in the blank: The intrinsic pathway of apoptosis is activated by _______.

Answer 27

[internal signal within the cell]

Question 28

Fill in the blank: The extrinsic pathway of apoptosis is activated by _______.

Answer 28

[external signal from outside the cell]

Question 29

What is psoriasis?

Answer 29

A chronic autoimmune condition resulting in the overproduction of skin cells.

Question 30

What happens during embryonic development in relation to apoptosis?

Answer 30

It shapes organs by removing excess cells.

Question 31

What is apoptosis?

Answer 31

Programmed cell death ## Footnote It occurs for cells that are infected, unnecessary, or unable to reproduce correctly.

Question 32

What is required for apoptosis to proceed?

Answer 32

An internal or external signal ## Footnote These signals initiate the apoptosis process.

Question 33

What are the physical changes that occur during apoptosis?

Answer 33

Cell shrinkage and blebbing to form apoptotic bodies ## Footnote These changes help in the orderly destruction of cells.

Question 34

How is the cell cycle normally regulated in a mature organism?

Answer 34

The rate of production of new cells balances the rate of loss of cells ## Footnote This balance is crucial for maintaining tissue health.

Question 35

What may result from the breakdown of the normal control of the cell cycle?

Answer 35

Cancers ## Footnote Cancer is a disease characterized by uncontrolled cell growth.

Question 36

How are cancerous cells characterized?

Answer 36

Unregulated rates of cell division ## Footnote This leads to tumor formation and other complications.

Question 37

what is the intrinsic/ mitochrondria stage

Answer 37

* inside the cell * caused by Dna damage, radiation, mitochrondrial stress, uv light or if a cell indentifies that is infected with a virus, internally.

Question 38

what triggers the intrinsic pathway

Answer 38

trigger proteins on the mitochrondria surface; activate mitochromdia breakdown relaeasing cytochromo C * when cytochromos are releasing from the mitochrondria they act as a signaling molecules to start apoptosis. * cytochromo C activates a secondary messenger that activates a caspase triggering the caspase cascade.

Question 39

what are the stages of intrinsic apoptosis

Answer 39

* activation of caspases *digestion of cell contents * cell shrinks * membrane blebbing and breakage

Question 40

step 1; activation of caspases

Answer 40

activation of caspases; the mitochrondria detect internal DNA damage and release **cytochromo C-** leading to the caspase cascade.

Question 41

step 2; digestion of cell contents

Answer 41

digestion of cell contents- caspases cleave intracellular proteins, which leads to the breakdown of organelles

Question 42

step 3; cell shrinks

Answer 42

cell shrinks- the cell and nucleus shrink as intracellular material is broken down.

Question 43

step 4; membrane blebbing and breakage

Answer 43

membrane blebbing and breakage; as the cytoskeleton is digested, the structural intergrity of the cell is weakened. * the membrane wraps and detaches from the cell in membrane-enclosed vesicles known as apoptotic bodies which contains the broken down intracellular material.

Question 44

what happens after apoptosis

Answer 44

after apoptosis phagocytes engluf and digest the free floating apoptotic bodies by phagocytosis

Question 45

definition of phagocytes and phagocytosis

Answer 45

Phagocytes are immune cells that engulf and digest foreign particles, bacteria, and cellular debris, including apoptotic cells after apoptosis. Phagocytosis, the process by which they engulf these materials, is crucial for maintaining tissue homeostasis and resolving inflammation.

Question 46

what is blebbing

Answer 46

a bleb is a bulge, or protrusion of the plasma membrane of a cell. eventually it will break off into vesicle-like strutures * little blebs can even form onto of big blebs * you can tell a cell is undergoing apoptosis when you see blebbing

Question 46

what is the extrinsic pathway/ death receptor

Answer 46

* outside the cell * intiated by a singalling molecule binding to a receptor outside the cell.

Question 47

the steps of the death receptor/extrinsic pathway

Answer 47

1. starts with ligand(primary signalling molecule, e.g. Fas Ligand(FASL)) being secreted by the a cytotoxic T-cell. 2. FasL binds to FasR (Fas Receptor) 3.the shape change attracts a molecule called FADD (Fas associated protein death domain) 4. this then attracts 2x prophase 8 molecules, these will then join togther to form caspase 8 5. caspase 8 attracts the substrate Procaspase 3 6. procasepase 3 is broken down into caspase 3 another enzyme!!! 7. caspase 3 cleaves (break up) proteins that make up the cytoskeleton of the cell (mircotubules) and the nucleus. 8. caspases also enter the nuclear membrane and degrade the proteins and DNA. 9. caspase 3 is therefore cleaving/breaking those proteins into fragments causing the cell to collapse and bleb.

Question 47

what are some similarities between the intrinsic and extrinsic pathway

Answer 47

both mechanisms set off a biochemical pathway that results in; * cell chrinkage * the eventual formation of apoptotic * the clean up of apoptotic bodies through phagocytosis ( after apoptosis) * the formation of blebs (protrusions of the cell mmbrane)

Question 48

what happens when apoptosis doesn't happen when it should?

Answer 48

apoptosis related malfunctions are the root cause of deviant cell production and some of the most deadly disease such as cancers * if cells live longer than they should, they accumulate mutations and are more likely to become cancerous. * sometimes things change in cells so that it deosn't respond to an apoptosis signalling molecule. * cancerous cells keep dividing until they form tumours **cancer treatment** * radiation thepary: radiation is meant to kill the cancer cells by triggering the intrinsic pathway. * chemothepary - multiple drugs given, some of which are likely to be synthetic 'death ligands' which bind to FasR on cell membrane and trigger the extrinsic pathway. - also may contain sythetic version of Smac protein - Smac proteins are relaeased in mitochrondria which triggers the release of cytochromo C from the mitochrondria. - other drugs that will prevent mitosis as well.

Question 49

what happens when apoptosis happen when it shouldn't?

Answer 49

* often leads to degenerative diseases such as Alzheimers, Parkinson's and huntington's disease. * lots of cell destrustion * often a generate cause as well, however the genetic cause may be related to a deffetcive protein involved in a apoptotic pathway. * HIV is a disease that is though to promote apoptosis!

Question 49

apoptosis and cancer

Answer 49

* cells may undergo certain changes that causes uncontrollable progress through the cell cycle * when cells do not undergo apoptosis they continue to grow and divide * they can pass on damaged DNA to daugther cells. This can lead to a number of disorders, including cancer.

Question 50

what is necrosis

Answer 50

necrosis is a traumatic cell death, the premature/ uncontrollable death of cells and tissues in the body due to injury, infection, or lack of blood supply. * it causes inflammation and affects surrounding tissue. * (mechanism) cells swell and rapture, releasing their contents into the surrounding tissues, triggering an inflammatory response. * (purpose) necrosis is a response to injury or disease, not a normal physiological process. Necrosis (accidental cell death) * (examples) cell death following a burn, a heart attack, or an infection * (significance) necrosis can lead to tissue damged, inflammation, and potential organ failure.