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Biochemistry and molecular science > Module 12 > Flashcards

Module 12 Flashcards

Genome maintenance

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Biology 101 flashcards
1
Q

What happens when gene maintenance go wrong

A

Cancer, deregulating cellular energetics, sustaining poliferative signalling, genome instability and mutation, replication immortality

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2
Q

What type of DNA damage can occur

A

chemical reaction
Spontaneous oxidative damage
hydrolytic attack (base is oxidise and removed, depruination)
uncontrolled methylation

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3
Q

What is an example of large disruptive lesion

A

Thymine dimers, hugely distorted by UV light, connecting two thymine together

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4
Q

Breaks in the DNA phosphate backbone

A

by ionising radiation, gamma ray

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5
Q

What error does polymerase pose

A

wrong base pairing, not base paired together properly(may end up with a permanent mutation.

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6
Q

What are the type of repair mechanism

A

Double strand break repair, nucleotide excision repair, single strand base excision repair, mismatch repair

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7
Q

What if lesion are not repaired

A

replication will stop and lose the whole strand.

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8
Q

What is a mutation

A

inheritable difference from the wildtype

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9
Q

Where must mutation be at for it to replicate

A

In the gametes or the cells that give rise to sperm and egg, or it need a large mutation for it to express it onto the nnext generation if it is else where(e.g skin cancer)

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10
Q

What is specific about mismatch repair

A

the method that is only specific to E. coli

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11
Q

What does mismatch repair do

A

methylation on the adenines in GATC sequence and hemimethylation on the new strand.

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12
Q

How to identify mismatch

A

using mut, cut the unmethylated side, exonuclease used to removed and polymerase to repair it.

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13
Q

What are the two similar repair systems

A

base excision repair(for small damage), nucleotide excision repair (for larger damage)

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14
Q

What is example of a damage to a single base

A

deamination, removed amine group and replaced with O, changed to uracil(from cytosine) or thymine (from 5-methylatedcytosine)

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15
Q

How to repair deamination

A

base excision repair, DNA glycosylase(uracil glycosylase if it is a uracil), then AP endonuclease to cut the backbone, DNA polymerase I will add the right base and use ligase to connect them

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16
Q

How to repair larger lerision

A

nucleotide excision repair, exonuclease cut 2 side, helicase used to hold them, DNA polymerase repair and ligase to close the nick

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17
Q

What causes double stranded break

A

Ionizing radiation, errors of DNA replication, oxidising agents, and other metabolites can cause breaks across both strands of the DNA

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18
Q

What is a error prone pathway or repair

A

repairs that contain large amount of errors (e.g double stranded break repair)

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19
Q

How does double stranded break repair

A

nonhomologous end joining, there are error because there are loss of nucleotide due to degration before end joining

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20
Q

What does G2 phase in cell cycle do

A

RNA and protein synthesis. No DNA synthesis

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21
Q

What does G1 phase in cell cycle do

A

RNA and protein synthesis, no DNA synthesis

22
Q

What is G0 phase

A

terminally differentiated cells withdraw from cell cycle indefinitely and may resume at G1 to start

23
Q

What controls the orderly process

A

Protein phosphorylation(inactivating and inactivating protein when phosphorylated), protein degration, protein synthesis, inhibitors(bind to protein to inhbit the protein)

24
Q

What control cell cycle

A

kinase, all use the same way to regulate, cyclin

25
Q

How is cyclin dependent kinases’s property

A

heavily regulated, stable protein levels across cell cycle, animals have 8 CDKs

26
Q

What is cyclin

A
  • Undergo a cycle of protein synthesis and degradation – protein levels are cyclical
  • Essential regulators of CDK activity • Are also regulated
  • Animals have 10 cyclins
  • Can be divided into G1/S cyclins, S-cyclins and G2/M cyclins
27
Q

What is mechanism 1 for regulating cell cycle

A

phosphorylation of CDKs, inactive, party active(active site is block) and fully active when it is bound to cyclin (allow target binding) Thr160 to activate and Tyr15 to inactivate (when phosphorylated)

28
Q

What are the types of cyclins

A

E-CDK2(G1-S), cyclin A-CDK2(S-M), cyclin B-CDK1(G2-M), cyclin D is through out

29
Q

Mechanism 2 for regulating the cell cycles

A

controlled degradation of cyclins, both tyr and thr are present, to allow it to activate quickly. positive regulate happens when phosphotase send signals then it will keep sending signal to produce for CDK(feebback loop). Negative feedback, binds to ubiquinine the more it activiate, to reduce it quickly.

30
Q

What is destruction box recognization protein for(DBRP)

A

destruction box is a 9 amino acid sequence near the amino terminus. marked for degradation. Use proteasome to recycle the chain to amino acid.

31
Q

Mechanism 3 for regulating the cell cycle

A

Regulated Synthesis of CDKs and cyclins

32
Q

Mechanism 4 for regulating the cell cycle

A

Protein inhibitors of CDK activity

33
Q

How does cyclin control them

A

by phosphorylating the target

34
Q

Example target in mitosis

A

nuclear lamins(in nuclear), it phosphorylate lamins to allow nuclear lamina to decondense, causing chromosome to condense.

Condensin, to condense DNA when mixed together, known to no longer to condense when mutated in condensins, physically interacting with DNA

35
Q

example of target in G1-S checkpoint control

A

Retinoblastoma(Rb), if there are damaged DNA are not repaired, it can pause the replication/mitosis or not completely replicated until it is repaired.

36
Q

How does retinoblastoma work

A

Rb binds to E2F, CDK2 becomes active and phosphorylate pRb to stop it from inhibiting to allow replication if DNA is perfect

37
Q

What is p53 for

A

cause inhibit p21 to be transcript when there is a break in the DNA. No longer be able to phosphorylate pRB, stop transcripting until the break is gone and p21 will degrade.

38
Q

What is retinoblastoma disease

A

cancer forms in retinal cells in both eyes, not fatal, loss of vision, Rb was tumour suppressor gene clone.

39
Q

What is sporadic cancer

A

cancer happen randomly, a cell with mutation and replicate until the pair of cell have both the mutation and it will produce a tumour.

40
Q

What if gene can never be used to replicate anymore

A

Programmed cell death, p53, breaking down of the cell and be engulfed, apoptosis

41
Q

What is the difference between necrosis and apoptosis

A

Necrosis is uncontrolled cell death that will burst open its content cause inflammatory response(too much errors). Apoptosis breakdown the contents inside and allow phagocytosis.

42
Q

Uses of apoptosis

A

sculpting, metamorph, killing nerve cell to refine neural connection, destroy unwanted immunoreponse.

43
Q

Why does tumour grow so fast,

A

They decreased in apoptosis, they dont die.

44
Q

Function of telomeres

A

maintains length of chromosomes

45
Q

What cell express telomerase

A
  • Most human cells do not express telomerase because they do not need to divide
  • Stem cells (cells to replenish other cells) express telomerase
  • Germ cells (that produce gametes) express telomerase
46
Q

What is senescence

A

terminal differentiation at approx 40-50 cell division, die if it divide further

47
Q

What happen when telomere gets too low

A

Cell will undergo massive cell death

48
Q

Difference of stem cells and somatic cells

A

stem cells contain telomerase to prevent degeneration, somatic cell dont not have telomerase

49
Q

What happens telomerase reactivate

A

It will have unlimited cell replication

50
Q

What is sunburn

A

radiation burn casing DNA damage triggers the production of melanin to protect further damage. if bad enough, it can trigger cell death pathways in the cell.

Biochemistry and molecular science (12 decks)

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