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biochem > Module 11 > Flashcards

Module 11 Flashcards

1
Q

Major forms of DNA damage

A
  • spontaneous oxidative damage
  • hydrolytic attack (more common for PURINES than PYRIMIDINES)
  • uncontrolled methylation

all damage to single base

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2
Q

Define DNA damage

A

any modification of DNA that changes its coding properties or natural function in transcription or replication

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3
Q

Define DNA mutation

A

an alteration in the nucleic acid sequence of the genome of an organism, virus, extrachromosomal DNA

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4
Q

Main causes of DNA damage

A
  • radio + chemotherapy
  • UV –> replication errors
  • light –> alkylating agents
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5
Q

What are the types of DNA repair mechanisms?

A
  • double-strand break repair
  • nucleotide excision repair
  • single-strand base excision repair
  • mismatch repair
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6
Q

What happens if a lesion is not repaired?

A

DNA replication will fail at that point & one part of the DNA will remain single-stranded

loss of a whole bunch of DNA

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7
Q

Explain how the mismatch repair identifies the incorrect base AFTER DNA replication

A

E coli is methylated on the adenines in GATC sequences

repairs single mismatches ONLY immediately after DNA replication

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8
Q

What is a possible cause of mismatch repair?

A

error during replication that was not corrected by the polymerase

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9
Q

What kind of proteins identify mismatches?

A

Mut proteins

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10
Q

What is depurination?

A

the HYDROLYTIC removal of GUANINE or ADENINE from the #1 carbon of deoxyribose in a DNA strand

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11
Q

What is deamination?

A

the HYDROLYTIC removal of amino (-NH2) groups from guanine, cytosine, or adenine

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12
Q

Damage to a single base

A
  • could remove a full base, or it could remove an amine group from a base –> deamination
  • hydrolytic attack removes AMINE GROUP
  • when this happens to cytosine, it becomes uracil (unusual)

5-methylcytosine –> thymine

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13
Q

What 4 enzymes are involved in base excision repair?

A

1) DNA glycosylase
2) AP endonuclease
3) DNA pol I
4) DNA ligase

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14
Q

What causes a thymine dimer?

A

UV

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15
Q

What are thymine dimers?

A
  • thymine dimers are 2 adjacent thymine bases that are abnormally linked together by covalent bonds
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16
Q

What is the consequence of thymine dimers?

A

this dimerization inhibits DNA replication, which may lend to death of organisms

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17
Q

What 4 enzymes are involved in nucleotide excision repair?

A

1) exinuclease
2) DNA helicase
3) DNA pol I
4) DNA ligase

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18
Q

What are 2 differences between base excision repair & nucleotide excision repair?

A

1) involves cutting at 2 sections on both sides of lesion

2) also removes the strand of DNA w/ lesion (nucleotide excision repair)

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19
Q

When is base excision repair needed?

A

a pathway that repairs replicating DNA THROUGHOUT the cell cycle

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20
Q

When is nucleotide excision repair needed?

A

a pathway that constantly repairs damaging DNA due to UV rays, radiation, & mutagens

21
Q

DS breaks are . . .

A

the most biologically significant lesions caused by ionizing radiation

22
Q

Most DS breaks are repaired within . . .

A

24 hours, but 25% of the repairs contain errors

ERROR-PRONE PATHWAY OF REPAIR (non-homologous end joining)

23
Q

Why is NHEJ error prone?

A

bc there will be a small loss of nucleotides due to the degradation from the ends (due to any nucleases that come into contact w/ them)

24
Q

4 main regulatory processes in the cell cycle

A
  • protein phosphorylation
  • protein degradation
  • protein synthesis
  • inhibitors
25
Q

What is special about the G0 phase?

A

terminally differentiated cells withdraw from the cell cycle at this point indefinitely (however, there is a re-entry point from G0)

26
Q

What are cyclin-dependent kinases?

A
  • regulates the PROTEINS that carry out cyclical cellular functions
  • are heavily regulated
  • require binding to a cyclin for activity
27
Q

Kinase activity is. . .

A

CYCLICAL

28
Q

What are cyclins?

A
  • undergo a cycle of protein SYNTHESIS + degradation
  • protein levels are cyclical
  • essential regulators of CDK activity (G1/S cyclins, S cyclins, G2/M cyclins)
29
Q

Phosphorylation of Thr160 . . .

A

in the T-loop ACTIVATES the CDK by allowing TARGET binding

30
Q

Phosphorylation of Tyr15, near the amino terminus. . .

A

INACTIVATES CDK2 by BLOCKING the ATP binding site w/ its negative charge

31
Q

What is DBRP?

A

destruction box recognizing protein

32
Q

What is the function of DBRP?

A

targets the cyclin for degradation

9 amino acid sequence neat the amino terminus

33
Q

What is ubiquitin?

A

small protein covalently bonded to proteins as a marker of degradation

34
Q

What is a proteasome?

A

large protein complex that degrades proteins back to amino acids

35
Q

What are the 2 CDK inhibitors?

A

p21 and p27

36
Q

What are 2 examples of CDK targets and the phase of the cell cycle at which they act?

A

1) Nuclear lamins

2) condensins

37
Q

What are nuclear lamins?

A

proteins found on inside of nuclear envelope

the breakdown of the nuclear envelope (during transition into mitosis) is assisted by the phosphorylation of the lamins by the CDKs that are controlling entry into mitosis

38
Q

What are condensins?

A

proteins that control the condensing of chromosomes

if you mix condensin proteins with DNA, they will naturally condense the DNA in the test tubes

39
Q

What happens if there are mutations in the condensins?

A

the cell can no longer condense its DNA

condensins are physically associated with the chromosomes

40
Q

Explain the importance of checkpoints in maintaining genome integrity

A

they ensure that a cell’s DNA is intact before permitting DNA replication & cell division to occur

41
Q

failures in these checkpoints can lead to . . .

A

an accumulation of damage, which in turn leads to mutations

42
Q

Why does inactivation of pRB lead to cancer?

A

riggers uncontrolled cell proliferation

43
Q

Cells with 2 altered copies of the RB1 gene produce. . .

A

NO functional pRB and are unable to regulate cell division effectively

retinal cells lacking functional pRB can divide uncontrollably to form cancerous tumours

44
Q

Describe some of the uses of programmed cell death during embryonic development

A

1) sculpting
2) refining neural connections
3) refining tissues - destroying self-recognizing B cells

45
Q

List 3 of the features of a cancer cell, so called “hallmarks of cancer”

A
  • resisting cell death
  • avoiding immune destruction
  • evading growth suppressors
46
Q

What causes a tumour?

A

increased growth

decreased apoptosis

47
Q

What is necrosis?

A

not programmed; the cell just bursts & that can lead to an inflammatory response

48
Q

Most cells don’t express telomerase enzyme. Which ones do?

A

1) stem cells (to replenish other cells)

2) germ cells (that produce gametes)

49
Q

What is pRB?

A

a tumor suppressor & key regulator of the cell cycle

biochem (9 decks)

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