BIO Most Important Processes Flashcards

1
Q

DNA Replication (4 steps)

A

MAKING MORE DNA
1) Helicase unwinds the double helix starting from the replication origin, separating the two polynucleotide strands by breaking the H-bonds between complementary base pairs.
2) The separated strands act as templates for the synthesis of new complementary strands.
3) Free deoxynucleotide triphosphates align opposite their complementary base partner.
4) DNA polymerase cleaves the two excess phosphates, using the energy released to link the nucleotide to the new strand.

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2
Q

DNA Transcription (4 steps)

A

MAKING AN mRNA COPY OF DNA (TO EVENTUALLY CREATE A PROTEIN)
1) RNA polymerase separates the DNA strands and synthesizes a complementary RNA copy from one of the DNA strands.
2) When the DNA strands are separated, ribonucleotide triphosphates align opposite their exposed complementary base partner.
3) RNA polymerase removes the additional phosphate groups and uses the energy from this cleavage to covalently join the nucleotide to the growing sequence.
4) Once the RNA sequence has been synthesized, RNA polymerase detaches from the DNA molecule and the double helix reforms.

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3
Q

DNA Translation

A

1) Ribosomes bind to mRNA in the cytoplasm and move along the molecule in a 5’ – 3’ direction until it reaches a start codon (AUG)
2) Anticodons on tRNA molecules align opposite appropriate codons according to complementary base pairing (e.g. AUG = UAC)
3) Each tRNA molecule carries a specific amino acid (according to the genetic code)
4) Ribosomes catalyse the formation of peptide bonds between adjacent amino
acids (via condensation reactions)
5) The ribosome moves along the mRNA molecule synthesizing a polypeptide chain
until it reaches a stop codon
6) At this point translation ceases and the polypeptide chain is released

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4
Q

PCR Process (3 steps)

A

1) Denaturation – DNA sample is heated to separate the two strands
2) Annealing – Sample is cooled to allow primers to anneal (primers designate sequence to be copied)
3) Elongation – Sample is heated to the optimal temperature for a heat-tolerant polymerase (Taq) to function and to extend the nucleotide chain from the primers

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5
Q

Phagocytosis (6 steps)

A

1) In response to infection, phagocytic leukocytes circulate in the blood and extravasate (move into the body tissues).
2) White blood cells are drawn to the site of infection by chemicals released by damaged tissues (e.g. histamine) via chemotaxis.
3) Pseudopodia (cellular extensions) surround a pathogen and fuse to form an internal vesicle, engulfing it.
4) This vesicle fuses to a lysosome, thus forming a phagolysosome, and the pathogen is digested.
5) Phagocytes may present antigens (pathogen fragments) on its surface to stimulate the third line of defense.

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6
Q

Development of adaptive immunity (6 steps)

A
  1. After phagocytic leukocytes enfulf a pathogen, some of them (dendritic cells) will present the antigens (digested fragments) on their surface.
  2. These dendritic cells migrate to the lymph nodes and activate specific helper T lymphocytes.
  3. These helper T cells release cytokines to activate the particular B cell capable of producing the complementary antibodies.
  4. The activated B cells divide and differentiate to produce short-lived plasma cells which produce a high amount of the specific antibody.
  5. These antibodies target the specific antigen, enhancing the capacity of the immune system to recognize and destroy the pathogen.
  6. Some of the activated B cells and helper T cells will develop into memory cells to provide long-lasting immunity.
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7
Q

Coagulation cascade (7 steps)

A

Step 1) Damaged cells and platelets release clotting factors which stimulate the cascade.
Step 2) Clotting factors cause platelets to activate and become sticky, adhering to the damaged region to plug up the wound.
Step 3) Clotting factors localize vasoconstriction, reducing blood flow and thus blood loss in the damaged region.
Step 4) Clotting factors catalyzes inactive zymogen prothrombin’s conversion into activated enzyme thrombin.
Step 5) Thrombin triggers the conversion of fibrinogen (soluble plasma protein) into fibrin (insoluble fibrous protein).
Step 6) Fibrin strands surround the platelet plug in an insoluble mesh of fibers to trap blood cells in a temporary clot.
Step 7) Once the damaged region is fully repaired, plasmin (enzyme) is activated to dissolve the clot.

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8
Q

Impulse to be transmitted across a synaptic cleft (6 steps)

A
  1. When an action potential reaches the axon terminal, it triggers the voltage-gated calcium channels to open.
  2. Calcium ions diffuse into the cells via these voltage-gated calcium channels and promote the fusion of vesicles containing neurotransmitters with the cell membrane.
  3. Neurotransmitters are released from the axon terminal via exocytosis and they cross the synaptic cleft.
  4. Neurotransmitters bind to specific receptors on the post-synaptic membrane and they open ligand-gated ion channels.
  5. Opening of ion channels generates an electrical impulse in the post-synaptic neuron which propagates the pre-synaptic signal.
  6. Neurotransmitters released into the synapse are recycled (by uptake pumps) or degraded by (enzymatic activity).
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9
Q

Acetylcholine creation, breakdown and reuptake (3 steps)

A

1) Acetylcholine is created from choline and acetyl CoA.
2) Acetylcholine is broken down by acetylcholinesterase (AChE, a synaptic enzyme) into its two component parts of VAChT and ChT. AChE is either released into the synapse from the presynaptic neuron or embedded on the membrane of the postsynaptic neuron.
3) The liberated choline is transported back into the axon terminal on the presynaptic neuron where it is coupled with another acetate group to reform into acetylcholine.

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10
Q

Depolarization (3 steps)

A

1) Sodium channels open within the membrane of the axon in response to a dendrite-initiated signal.
2) The opening of sodium channels causes a passive influx of sodium since sodium ions are more concentrated outside of the neuron.
3) This influx of sodium results in the membrane potential becoming more positive (depolarization).

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11
Q

Repolarization

A

1) Potassium channels open within the membrane of the axon, following an influx of sodium.
2) The opening of potassium channels causes a passive efflux of potassium since potassium ions are more concentrated inside the neuron.
3) This efflux of potassium causes the membrane to return to a more negative internal charge (repolarization).

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12
Q

Refractory period (hyperpolarization) - 3 steps

A

1) In a normal resting state (resting potential), sodium ions are in greater concentration outside the neuron and potassium ions are in greater concentration inside.
2) Following depolarization (sodium influx) and repolarization (potassium efflux), this ionic distribution is largely reversed.
3) The resting potential must be restored via the antiport action of the sodium-potassium which allows the neuron to fire again.

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13
Q

Action potential along an axon (4 steps)

A

1) When ion channels open, they cause the membrane potential to depolarize.
2) The ion channels that occupy the length of the axon are voltage-gated and open in response to changes in membrane potential.
3) As such, depolarization at one point of the axon triggers the opening of ion channels in the next segment of the axon.
4) This causes depolarization to spread along the length of the axon as a unidirectional ”wave”.

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14
Q

Muscles used for inspiration

A

1) The diaphragm muscles contract, which causes the diaphragm to flatten and increase the volume of the thoracic cavity.
2) The external intercostals contract, which pull the ribs outwards and upwards, expanding the chest.
3) Additional muscle groups (e.g. sternocleidomastoid, pectoralis minor) may help pull the ribs up and out.

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15
Q

Muscles used for exhalation

A

1) The diaphragm muscles relax, which causes the diaphragm to curve upwards and decrease the volume of the thoracic cavity.
2) The internal intercostal muscles contract, which pull the ribs inwards and downwards, reducing the breadth of the chest.
3) The abdominal muscles contract and push the diaphragm upwards during forced exhalation.
4) Additional muscle groups (e.g. quadratas lumborum) may help pull the ribs downwards.

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16
Q

Absorption of triglycerides

A

The digestion of triglycerides differs from other molecules because they must be:
1) emulsified by bile to be transported across the cell membrane as micelles by passive diffusion before reforming back into triglycerides.
2) These fatty globules combine with proteins in the Golgi, forming a chylomicron which is then
3) exocytosed from the cell and enters the lacteal
4) to be absorbed into the lymphatic system, rather than the usual circulatory systems, and transported away from the intestine.

17
Q

Glucose absorption

A
  1. Glucose is moved into the intestinal epithelial cells by cotransport with sodium ions.
  2. It then travels a short distance into the bloodstream. The capillaries near these cells have large pores that glucose can directly pass through.
  3. Glucose moves towards the hepatic portal vein and to the liver, where the excess glucose can be stored as glycogen.
18
Q

Starch breakdown

A
  1. Amylase starts digesting amylose and amylopectin by breaking the 1,4 bonds in both. This transforms it into maltose (two glucose) and maltotriose (three glucose).
  2. Small fragments of amylopectin (held together by 1,6 bonds) that cannot be digested by amylase are called dextrins.
  3. Maltase digests maltose, glucosidase digests maltotriose, and dextrinase digests dextrin.
19
Q

Phases of the cell cycle (interphase)

A

G1) 1st intermediate gap stage in which cell grows and prepares for DNA replication
S) Synthesis stage in which DNA is replicated
G2) 2nd intermediate gap stage in which the cell finishes growing and prepares for cell division
Mitosis) Nuclear division (DNA is separated into two identical nuclei)
Cytokinesis) Cellular contents are segregated and split in two