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Molecular Diagnostics > DNA Damage And Repair > Flashcards

DNA Damage And Repair Flashcards

1
Q

What are examples of exogenous causes of DNA damage?

A

-Thermal disruption
-UV light exposure
-Ionizing Radiation
-Exposure to mutagens, carcinogens, and viruses

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2
Q

What are examples of endogenous causes of DNA damage?

A

-Cellular metabolism
-Hydrolysis
-Nuclease digestion

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3
Q

What are outcomes of DNA damage?

A

-DNA repair, direct reversal
-DNA repair, excision. Repair
-Apoptosis (programmed. Cell death)
-Senescence (old cell)
- Cell with DNA. Damage retained. (Worse case)

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4
Q

What are the types of DNA damages?

A

-Single. Strand breaks
-Double strand breaks
-Pyrimidine. Dimer
-Nucleotide base oxidation

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5
Q

Examples of ionizing radiation are?

A

Gamma rays. And X-rays

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6
Q

What is the wavelength of UV-C rays?

A

~260 nm

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7
Q

What ultraviolet rays are absorbed by DNA?

A

UV-C, and UV-B

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8
Q

What are three chemical products in the environment that may cause DNA damage?

A

Hydrocarbons, aflatoxins, and chemotherapy

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9
Q

A source of hydrocarbon can come from…?

A

Cigarette smoke

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10
Q

Most error during DNA replication by error of?

A

Polymerase 3’ to 5’ exonuclease activity

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11
Q

MMR enzyme mutation. Caused ________

A

Mismatch repair failure

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12
Q

Highly - reactive oxygen radicals

A

A build up of reactive oxygen species in cells may cause damage to DNA, RNA, and proteins, and may cause cell death

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13
Q

The human genome project revealed ____ genes whose products participate in _____ _____.

A

130 genes, DNA repair

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14
Q

What is DNA photolyase?

A

Directly reverse cyclobutane pyrimidine dimer (CPD) via photochemical reactions. This is used in the natural repair system for pyrimidine dimers caused by UV damage.

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15
Q

What is excision repair?

A

Damaged base or bases removed and replaced with correct bases in a localized burst of DNA synthesis.

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16
Q

What is MGMT?

A

Stands for O^6-methylguanine-DNA methyltransferase. It prevents mismatch and errors during DNA replication and transcription.

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17
Q

What is the significance of the methylation state of MGMT gene promoter?

A

It determines whether tumor cells. Would response o temozolomide drug therapy.

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18
Q

In base excision repair, what enzyme removes incorrect nucleotides?

A

DNA glycosylase. There are at least 8 different genes encoding different DNA glycosylase.

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19
Q

In base excision repair (BER), what enzyme is responsible for replacing the missing nucleotide with the correct one?

A

DNA polymerase beta, one of at least 11 DNA polymerases encoded by genes.

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20
Q

What is required for the ligation of a break in the strand of DNA?

A

ATP is required.

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21
Q

Nucleotide. Excision repair repairs by…

A

Removing a large “patch” around the damage.
Example would be removing DNA damage induced by UV (thymine dimer)

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22
Q

In nucleotide excision repair what do Xp products do?

A

They repair DNA damage by cutting DNA both the 3’ side and 5’ side of the damaged area so tract containing damage can. Be removed.

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23
Q

In nucleotide excision repair, what enzymes are used to replace the wrong nucleotide with the correct one? This is after the wrong nucleotides have been removed.

A

Polymerase delta and polymerase epsilon

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24
Q

UV light may cause what in DNA?

A

Thymine dimer

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25
Q

What is xeroderma pigmentosum (XP)?

A

Rare inherited autosomal recessive disease of humans in which a deficiency of excinuclease occurs. It manifest as skin discoloration and multiple tumors on exposure to UV light.

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26
Q

What could cause xeroderma pigmentosum?

A

Mutations in several genes, XPA, XPB, XPF, and XPG which play a role in nucleotide excision repair (NER)

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27
Q

Unrepaired pyrimidine dimmers in humans may lead to…

A

Melanoma

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28
Q

What is mismatch repair (MMR)

A

A system for recognizing and repairing erroneous insertion, deletion, and mis-incorporation of bases that can arise during DNA replication and recombination, as well as repairing some forms of DNA damage. In other words deal with correcting mismatching nucleotides.

29
Q

What are important steps in mismatch repair (MMR)?

A

Recognition of mismatch using several proteins.
Cutting the mismatch out

30
Q

What gene encodes the caretaker gene important in mismatch repair (MMR)?

A

MSH2 also known s MutS protin homologous 2

31
Q

What gene encodes for the protein that helps cut out mismatch nucleotides in mismatch repair (MMR)?

A

MutL homologous. It forms a complex with MutS and MutH

32
Q

Mutations in MutS, MutH, or MutL will predispose a person to inherit what kind of cancer?

A

Colon cancer

33
Q

MutL, MutS, and MutH can also be called…

A

Tumor suppressor genes

34
Q

Single Strand breaks are repaired by?

A

BER, NER, and MMR. They are all strand specific SSB repairing system

35
Q

Double strand breaks (DSBs) are repaid by

A

Double strand breaks described as complete break in DNA. They are repaired by rejoining the DNA (direct joining) or homologous recombination.

36
Q

A double strand breaks and DNA strands are joined together with some complementary nucleotide is what kind of joining?

A

Nonhomologous End-Joining (NHEJ)

37
Q

What is homologous recombination?

A

Also known as homologous directed repair (HDR). Recombining chromatids during G2 or homologous chromosome in G1.

38
Q

What are the two genes responsible for coding the proteins used in homologous recombination?

A

BRCA1 and BRCA2

39
Q

If there are mutations in BRCA1 and BRCA2 that render protein produced defected this will predispose patients for?

A

Predispose women to breast and ovarian cancer

40
Q

List the cell cycle in order

A

G0, G1, S, G2, Mitosis (M)

41
Q

What are the cycles within M (mitosis) phase of the cell cycle? Put in order

A

Prophase, metaphase (checkpoint), anaphase, telophase, and cytokinesis

42
Q

What are the three check points in the cell cycle?

A

G1, G2, and Metaphase of the M phase.

43
Q

Describe G0

A

Resting phase where cell has left cycle and has stopped dividing

44
Q

Describe G1

A

Cells increase in size. The G1 checkpoint control mechanism happens to ensure everything is ready for DNA synthesis

45
Q

Describe S phase of the cell cycle

A

DNA replication occurs during this phase

46
Q

Describe G2 phase

A

Gap between DNA synthesis and mitosis continues. G2 check point happens to ensure everything is ready to enter the M (mitosis) phase and divide.

47
Q

Describe M phase of the cell cycle

A

Cell growth stops and cellular energy s focused on the orderly division into two daught cells. Checkpoint in the middle of mitosis (metaphase) ensures cell is ready to complete cell division

48
Q

What are the major proteins that control the cell cycle?

A

Cyclin-dependent protein kinases (Cdks) and cycling

49
Q

Cdk-cyclin complex will do what?

A

Ability of Cdk to “P” target is dependent on the cyclin that it forms a complex with

50
Q

In the cell cycle, P53-p21 activation will mean what?

A

Prevents cell from transitioning to the S phase (from G1).

51
Q

Activation of cyclin D-cdk4 will do what?

A

Phosphorylation of retinoblastoma protein (pRb) in the nucleus.

52
Q

If retinoblastoma protein (RB) remains unphosphorylated what will happen?

A

Unphosphorylated retinoblastoma will inhibit G1 by preventing E2F-mediated transcription

53
Q

DNA damage during G2 phase will cause what to happen?

A

Initiates a signaling cascade that regulates wee1 and cdc25 activity, therefore controlling mitosis entry via cyclin B-cdk2 that can delay mitotic entry

54
Q

What protein is responsible for ensuring chromosomes are properly attached to the spindle?

A

P53-cdk2-GADD45

55
Q

If P53-cdk2-GADD45 is activate what will happen in the mitotic checkpoint of the cell cycle?

A

The cell will not go to the anaphase because the spindles are not properly connected to the chromosomes.

56
Q

What s apoptosis?

A

Programmed cell death

57
Q

What are some characteristics of a cell undergoing apoptosis?

A

Blabbing, cell shrinkage, nuclear fragmentation, chromatin condensation, chromosomal DNA fragmentation, and local mRNA decay

58
Q

What are two significant apoptotic genes?

A

BCL2 and TP53

59
Q

What is BCL-2 known for?

A

It’s role in inhibiting apoptosis (works with BAX and BAK) and promotes oncogenesis such as FL

60
Q

What is follicular lymphoma (FL)?

A

Uncontrolled cell division of B-cells known as centrifuges and center oblasts. Cells normally occupy follicles in germinal centers of lymphoid tissues.

61
Q

What are some evidence a cell is undergoing necrosis?

A

Increase cell volume
Loss of plasma membrane integrity
Leakage of cellular contents

62
Q

What are clinical features of xeroderma pigmentosum?

A

Skin tumors, photosensitivity, cataracts, and neurological abnormalities

63
Q

What are clinical features of cockayne syndrome?

A

Reduced stature, skeletal abnormalities, optic atrophy, deafness, photosensitivity, and mental retardation

64
Q

What are clinical features of Fanconi anemia?

A

Anemia, leukemia susceptibility, limb, kidney, and heart malformations, chromosome instability

65
Q

What are clinical features of bloom syndrome?

A

Growth deficiency, immunodeficiency, chromosome instability, increased cancer incidence

66
Q

What are clinical features of Werner syndrome?

A

Cataracts, osteoporosis, atherosclerosis, loss of skin elasticity, short stature, diabetes, increase cancer incidence, sometimes described as premature aging

67
Q

What are the clinical features of ataxia-telangiectasia?

A

Cerebella’s ataxia, telangiectases, immune deficiency, increased cancer incidence, and chromosome instability

68
Q

Clinical features of hereditary nonpolyposis colorectal cancer?

A

Proximal bowel tumors, increased susceptibility to several other types of cancer.

Molecular Diagnostics (6 decks)

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