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Bio II > Lecture 21: DNA Damage and Repair > Flashcards

Lecture 21: DNA Damage and Repair Flashcards

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1
Q

How many damage events does a cell’s genome sustain per day?

A

1,000 to 1,000,000

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2
Q

What several types of DNA damage are possible?

A
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3
Q

What are some possible sources of DNA damage?

A
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4
Q

Spontaneous damage vs Induced damage

A
  • Spontaneous damage is caused by normal cell processes.
  • Induced damage is caused by environmental agents.
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4
Q

What are internal signaling pathways are cell responses to damage?

A
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5
Q

What does this represent?

A

Some most common types of spontaneous DNA damage

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6
Q

About how many time does spontaneous hydrolysis in bases happens per day and needs to be repaired?

A

100-1000

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7
Q

What can ethylmethane sulfonate (EMS) do?

A

it is and an alkylating agent that can donate an alkyl group such as methyl or ethyl in a group transfer reaction.

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8
Q

What can the alkylation of a nucleotide base do?

A

changes its structure and chemical properties in
DNA. Can results in a GC to AT substitution mutation

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9
Q

What are used to fix different types of DNA damage?

A

Several DNA repair systems with proteins that play different roles in each.

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10
Q

What induces pyrimidine dimers?

A

UV light

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11
Q

What are pyrimidine dimers?

A
  • Covalent bond between thymine or cytosine bases produced via a photochemical reaction.
  • Creates a kink in the secondary structure that stalls the enzymes responsible for transcription and DNA replication.
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12
Q

What repairs pyrimidine dimers?

A

the NER system (nucleotide excision repair system)

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13
Q

In which types of organisms is NER needed?

A

both eukaryotes and and prokaryotes

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14
Q

What are the fir steps of the nucleotide excision repair system?

A
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15
Q

What type of protein is necessary for step 1?

A

sensor protein

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16
Q

What type of protein is necessary for step 2?

A

endonuclease

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17
Q

What type of protein is necessary for step 3?

A

DNA polymerase

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18
Q

What type of protein is necessary for step 4?

A

ligase

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19
Q

Is a primase necessary in the NER system?

A

no

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20
Q

Where are the three checkpoints on the cell cycle?

A
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21
Q

What is needed to pass the G1 checkpoint?

A

*Growth factors (signals from other cells) are present
*Nutrients are sufficient
*Cell size is adequate
*No DNA damage

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22
Q

What is needed to pass the G2 checkpoint?

A

*Chromosome replication is successfully completed
*No DNA damage

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23
Q

What is needed to pass the M checkpoint?

A

All chromosomes are attached to mitotic spindle

24
Q

Hoe does the cell cycle checkpoints assess the integrity of the genome?

A
  • One of major assessment of cell cycle = looking for DNA damage
  • if detected, cell cycle is stalled (aka cell cycle arrest)
  • cell activates repair systems & try to repair damage
25
Q

What are the steps of apoptosis?

A
  1. Cell shrinks.
  2. DNA is fragmented.
  3. Membrane forms
    protrusions (blebs).
  4. Cell breaks up into small
    membrane-enclosed sacs
    (apoptotic bodies).
  • Phagocytic immune cells
    destroy the apoptotic bodies.
26
Q

What is a mutation?

A

a change in the DNA sequence of an organism’s genome

27
Q

How are mutations important in evolution?

A

Mutations provide genetic variation, which is essential for natural selection and the evolution of species.

28
Q

How are mutations important in disease?

A

Mutations can lead to genetic disorders or contribute to the development of diseases

29
Q

Compare somatic mutations and germ-line mutations

A
30
Q

Which genome sequences are affected by mutation?

A

Any sequence can be involved in a mutation.

30
Q

What is the consequence of a mutation affecting the sequence encoding amino acids of a polypeptide?

A

mutation
can affect the structure and function of the protein.

31
Q

What is the consequence of a mutation affecting the sequence encoding nucleotides of an RNA gene product?

A

mutation can affect the structure and function of the RNA.

32
Q

What is the consequence of a mutation affecting Gene Control Elements?

A

mutation can influence gene
expression.

33
Q

What causes mutations in a cell?

A

by random events in a cell

34
Q

What are mutations the result of?

A

errors in DNA replication or DNA recombination during cell division

35
Q

What can increase the frequency of mutations?

A

with exposure to mutagens.

36
Q

What are mutagens?

A

chemical or physical agents that can cause DNA damage

37
Q

What are the units for mutation rates?

A

mutations per [DNA unit] per [replication unit]

or

mutations per base pair per generation

38
Q

Compare mutation rates of prokaryotes and eukaryotes

A

similar (low) between
prokaryotes and eukaryotes.

39
Q

In what type of organisms are mutations rates the highest?

A

in RNA viruses and other RNA based infectious agents (viroids).

40
Q

What are the four types of large-scale mutations?

A
41
Q

What type of mutation is this an example of?

A

Large-scale mutation: A translocation associated with a type of leukemia (blood cell cancer).

42
Q

Which set of chromosomes is a cancer cell’s one? How can you tell?

A

right side, Cancer cells accumulate several large scale mutations and contain abnormal numbers of chromosomes.

43
Q

How are the three types of small-scale mutations categorized?

A

based on their effect on DNA structure.

44
Q

What are the three types of small-scale mutations?

A
  1. Nucleotide pair Substitution
  2. Nucleotide pair Insertion
  3. Nucleotide pair Deletion
45
Q

What are point mutations?

A

Small-scale mutations that involve one nucleotide pair

46
Q

Which type of DNA damage is this?

A

Base-pair mismatch

47
Q

Which type of point mutation resulted after cell division?

A

. Nucleotide pair Substitution

48
Q

Cytosine will base pair with guanine normally, but thymine and uracil will base pair with ___________ .

A

adenine

49
Q

What can happen if base deaminations in DNA go undetected and unrepaired during cell division?

A

it can lead to a mutation
in one of the daughter cells that
can then be propagated.

50
Q

Give examples of the phenotypes caused by DNA damage repair genetic diseases

A

range from neurological dysfunction, immunodeficiency, reproductive and growth defects, premature ageing, and cancer

51
Q

How were repair systems and their protein components in
humans discovered?

A

by the analysis of these genetic
diseases that affect DNA repair.

52
Q

Why would an abnormal DDR* (due to mutation) be associated with cancer predisposition?

*DNA Damage Response

A

because it compromises the cell’s ability to repair DNA damage efficiently.

This increases the likelihood of accumulating mutations over time, which can lead to the uncontrolled cell growth characteristic of cancer.

53
Q

What is Xeroderma pigmentosum (XP)?

A

rare autosomal recessive disease in humans caused by a defect in NER.

54
Q

What causes XP (Xeroderma Pigmentosum)?

A

mutations in one of eight genes that produce the eight proteins involved in NER (Nucleotide Excision Repair)

55
Q

What effect do mutations in XP genes have?

A

they produce non-functional proteins. Individuals with two copies of a non-functional allele for one of these proteins have a non-functional NER system.

56
Q

How is XP characterized?

A

by photosensitivity, the development of skin lesions, pigmentation abnormalities, precancerous lesions, and a high predisposition to developing skin cancer.

57
Q

Why are XP patients sensitive to UV lights?

A
  • UV light produces pyrimidine
    dimers in DNA that are normally
    repaired by the NER system.
  • XP individuals cannot repair this
    type of damage (e.g., thymidine
    dimer) typically repaired by the
    NER system and are sensitive to
    UV light.

Bio II (21 decks)

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