Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

BMS > Introduction to Nucleic Acids, DNA, Chromatin and Chromosome Structure > Flashcards

Introduction to Nucleic Acids, DNA, Chromatin and Chromosome Structure Flashcards

1
Q

Store and express genetic information and transmit it from one generation to the next

-Confer individuality

A

Nucleic Acids (DNA and RNA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Joins DNA segments to form hybrid molecules

Ex: Chromosome crossing over during meiosis and the diversity of B cells

A

Recombination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Every cell contains the exact same DNA, but the diversity comes from the

A

Expression of that DNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What nucleotide component actually carries the genetic information?

A

The base

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How can we combat the bacteria Salmonella typhimurium?

A

Inactivtion of DNA adenine methylase (dam)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Blocks expression of virulent genes, prevents disease development, and induces an immune response

A

Inactivation of dam

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Incorporated in the DNA during replication and block further DNA synthesis

-does not significantly affect the host cell metabolism

A

Nucleoside analogs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Hydrolyze phosphodiester bonds

A

Nucleases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the most common form of DNA?

A

B DNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

States that there must be equal amounts of purines and pyrimidines in the double-stranded DNA

A

Chargaff’s rule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Each diploid cell contains how many chromosomes?

A

46 (6ft of DNA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Linear or circular B-form double helix

A

Relaxed conformation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Has fewer helical turns than the relaxed B-form DNA double-helix

-classified as anything less than 10 helical turns

A

Negative supercoil

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Negative supercoils are energetically favored. The energy needed for strand separation is stored in

A

Supercoils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Force the eukaryotic DNA to wrap around them and generate a negative supercoil

A

Histones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Change the tertiary structure of DNA by transiently breaking one or both DNA strands, passing the strands through the break, and rejoining the strands

-induces “swivel points” in the DNA helix

A

Topoisomerases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Why do we need topoisomerases?

A

Positive supercoiling is too much tension, so topoisomerases come in and release the tension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How are topoisomerases able to work?

A

They have nuclease and ligase activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What makes DNA gyrase (a Topo II) unusual?

A

It can induce negative super coils into relaxed DNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Why is inhibition of DNA gyrase a good strategy for antibiotics?

A

It inhibits bacterial DNA syntheis, and since Eukaryotes do not have DNA gyrase, there are no side effects for humans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Inhibition of eukaryotic Topoisomerases is used in cancer treatment, this has signigicant side effects because it will

A

Lead to cell death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

DNA is associated with non-histone proteins and condensed into a non-membrane bound nucleoid in

A

Prokaryotes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

DNA is associated with histone and non-histone proteins and is condensed into a nucleoprotein complex called chromatin in

A

Eukaryotes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Chromatin is arranged in repeating units (like beads on a string) called

A

Nucleosomes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the structure of a Nucleosome

A
  1. ) Core: made up of DNA supercoils and histones

2. ) DNA spacer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

20-80 bp of DNA between cores

-binds H1

A

DNA spacer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

The regional compaction of chromatin is affected by

A

Histone modifications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

As soon as DNA replication is completed, one histone H1 binds the spacer DNA which promotes

A

Tight packing (Solenoid)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

In prokaryotes, replication is initiated by strand separation at a location rich in A:T base pairs, called the

A

Origin of replication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

DNA unwinding is catalyzed by DNA helicase within the

A

Pre-priming complex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Bind DNA cooperatively to keep the single strands apart and protect them from nucleases

A

Single-strand DNA-binding proteins (SSBs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What would be the affect of an inhibitor of Helicase?

A

Inhibited progression of DNA replication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

DNA polymerase can not initiate synthesis on a totally single-stranded template. As a result, it requires an

A

RNA primer

34
Q

Can replaced mismatched nucleotides that escaped proofreading after DNA replication

A

Mismatch Repair (MMR) pathway

35
Q

Has 5’ to 3’ exonuclease activity, which it uses to remove RNA primers from Okazaki fragments before it fills in the gap with DNA

A

DNA polymerase I

36
Q

ATP dependent enzyme that covalently joins Okazaki fragments

A

DNA ligase

37
Q

Contains primase and initiates syntheses on the leading and lagging strand in eukaryotic replication

A

DNA polymerase α

38
Q

DNA polymerase α has no

A

Exonuclease activity

39
Q

Responsible for DNA replication on the lagging strand in eukaryotes

  • associates with proliferating cell nuclear antigen (PCNA)
  • has 3’ to 5’ exonuclease activity
A

DNA Polymerase δ

40
Q

Responsible for DNA synthesis on the leading strand in eukaryotes

  • associates with processivity factor of PCNA
  • has 3’ to 5’ exonuclease activity
A

DNA Polymerase ε

41
Q

Displaces the 5’ ends of primers from Okazaki fragments

A

DNA Polymerase δ

42
Q

Consist of short non-coding G-rich DNA repeats (TTAGGG) and associated proteins

  • form T loops
  • Located at ends of linear chromosomes
A

Telomeres

43
Q

Protect the ends of DNA from recognition as broken DNA and degredation

A

Telomeres

44
Q

A ribonucleoprotein complex that adds short G-rich DNA repeats (TTAGGG) to the single stranded 3’-ends of linear chromosomes

A

Telomerase

45
Q

Uses it’s RNA component to extend the parent strand and then its protein component (with reverse transcriptase activity) to synthesize DNA

A

Telomerase

46
Q

Implicated in cell aging and cancer

A

Telomerase

47
Q

In most somatic cells, telomerase is inactive. So to prevent telomere shortening and eventual chromosome end-to-end fusion, p53 induces

A

Cell growth arrest (stops cell from replication)

48
Q

Can limit human cancer cell proliferation

A

Telomerae inhibitors

49
Q

Inherited disease caused by reduced Telomerase activity

-affects precursor cells in highly proliferative tissues

A

Dyskeratosis Congenita

50
Q

Patients with Dyskeratosis Congenita generally die from

A

Bone marrow failure

51
Q

Rare inherited condition that shows accelerated telomere shortening

-Patients generally die from a myocardial infarction before age 20

A

Hutchinson-Gilford Progeria

52
Q

Incorporation of an incorrect nucleotide or of an extra nucleotide

-None of the nucleotides are defective

A

Mismatch

53
Q

When there is a damaged base, the Base Excision Repair (BER) pathway is activated, what does it do?

A

Damage base removed, sugar backbone is cut and sugar phosphate residue is removed. Gap is pilled by DNA polymerase

54
Q

Repair proteins, recognize mismatches, and distinguish the newly synthesized strand with the error from the parental strand

A

Mismatch Repair pathway (MMR)

55
Q

In prokaryotes, a mismatched DNA is recognized because it is

A

Not immediately methylated

56
Q

How does MMR work?

A

Helicase and exonuclease remove the mismtched DNA and DNA poylmerase III fills the gap

57
Q

90% of lynch ryndrome patients have mutations in

A

MSH2 or MLH1 (MMR proteins)

58
Q

Reactive oxygen species (ROS), by-products of cellular metabolism and certain chemicals can cause damage to the bases in our DNA. This damage is corrected by the

A

Base Excision Repair pathway (BER)

59
Q

Mutation that interfere with BER lead to a high risk of

A

Colon cancer

60
Q

Premature aging disease caused by the inhibition of WRN helicase, which is involved in the BER

A

Werners Syndrome

61
Q

Cigarette smoke contains carcinogens. Once oxidized, these compounds covalently bind to G residues in the DNA of lung cells and distort the helix. What pathway would be used to fix this?

A

Nucleotide excision repair pathway

62
Q

The only mechanism that removes bulky DNA adduct

A

Nucleotide Excision repair

63
Q

Used if adduct is in a transcriptionally inactive region of DNA

-Highly associated with cancer

A

Global Genomic NER

64
Q

Used if adduct is in a transcriptionally active region of DNA

-associated with CNS disorders

A

Transcription-coupled NER

65
Q

Xeroderma pigmentosum, a hereditary disorder resulting from defects in global genomic NER, results in extreme

A

Solar sensitivity and highly increased risk of skin cancer

66
Q

Adducts in transcriptionally active regions of DNA block the progression of

-Halts gene transcription

A

RNA polymerase II

67
Q

Hereditary developmental and neurological disorder associated it defects in TC-NER where there are mutations in CSA or CSB which affects recognition of stalled RNA polymerase II

A

Cockayne syndrome

68
Q

Unlike patients with Xeroderma pigmentosum, patients with Cockayne Syndrome are not at increased risk for

A

Skin cancer

69
Q

Repairs errors commonly caused by oxidative damage that results in a break in one strand of the DNA that is typically missing a single nucleotide

A

Single-strand break repair pathway

70
Q

A single strand break is first recognized by

-Recruits XRCC1

A

PARP-1

-Poly(ADP-ribose) polymerase 1

71
Q

Restores the proper 3’ OH and 5’ phosphates of the damaged DNA which enables beta-polymerase to insert the missing nucleotide

A

Aprataxin (APTX)

72
Q

Ataxia Oculomotor Apraxia is an autosomal recessive spinocerebellar ataxia syndrome caused by mutation in the

A

APTX gene

73
Q

Severely compromise genome stability and lead to loss of chromosome fragments in mitosis

-Cause cancer due to joining of the wrong ends

A

Double-stranded breaks

74
Q

The major pathway to repair double-stranded breaks. Rejoins what remains of two broken DNA ends

  • Does not require any sequence homology
  • error prone
A

Non-homologous end-joining (NHEJ)

75
Q

In NHEJ, frayed ends are removed (if needed) by the endonuclease activity of

A

DNA-PKcs:Artemis

76
Q

Information on the homologous sequence is used to repair the broken DNA

-requires alignment of highly homologous DNA molecules

A

Homologous recombination

77
Q

Results in no change in DNA sequence

-error free

A

Homologous recombination

78
Q

Mutation in homologous recombination proteins BRCA1 or BRCA2 leads to an 80% lifetime risk of developing

A

Breast or Ovarian Cancer

79
Q

Tumors in BRCA carriers are more sensitive to

-due to defects in DSB HR repair

A

Ionizing radiation

80
Q

Ataxia Telangiectasia is an autosomal recessive disorder that has a propensity to develop lymphoid cancer. It is associated with a mutation in a protein that is normally activated by double stranded breaks. The protein signals the cell-cycle check point to slow the cell cycle. What is this protein?

A

AMT

BMS (62 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions