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Molecular Foundations of Medicine > DNA > Flashcards

DNA Flashcards

1
Q

nucleotide vs. nucleoside

A
  • nucleotide has nitrogenous base, sugar, and phosphate group
  • nucleoside has only the base and sugar. NO phosphate group
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2
Q

pyrimidines

A
  • have one ring

* PY-CUT- cytosine, thymine, and uracil

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3
Q

purines

A
  • 2 rings

* Pur As Gold: adenine and guanine

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4
Q

nucleotides synthesized as

A
  • synthesized as monophosphates

* then converted to triphosphate form and added to DNA

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5
Q

DNA methylation-
What is it?
Significance?
effect in humans?

A
  • methyl group added to cytosine
  • occurs in segments with CG patterns (“CG islands”)
  • inactivates transcription
  • human DNA ~70% methylated
  • unmethylated CG can stimulate immune response
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6
Q

Bacterial DNA methylation

A
  • methylate cytosine and adenine
  • it protects them from bacteriophages
  • non-methylated DNA destroyed by endonucleases
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7
Q

Chromatin

A
  • =DNA+proteins

* units of chromatin condense into chomosomes

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8
Q

nucleosome

A

=units of histones + DNA

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9
Q

Histones

A
  • H1, H2A, H2B, H3, H4
  • high content of lysine and arginine
  • positively charged -> binds negatively charged phosphate backbone
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10
Q

H1

A
  • distinct histone
  • not in nucleosome core, larger and more basic
  • ties beads on string together
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11
Q

Drug induced lupus

A
  • fever, joint pains, rash after start drug
  • Anti-histone antibodies
  • Classic drugs: hydralazine, procainamide, isoniazid
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12
Q

Classic Lupus

A

anti-dsDNA antibodies

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13
Q

heterochromatin

A
  • condensed
  • gene sequences not transcribed
  • significant DNA methylation
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14
Q

Euchromatin

A
  • less condensed
  • transcription active
  • significant histone acetylation
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15
Q

histone acetylation

A
  • acetyl group added to lysine

* relaxes chromatin -> transcription

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16
Q

histone deacetylation

A
  • packs chromatin more tightly

* blocks transcription

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17
Q

Histone Deacetylase inhibitors (HDACs)

A

•potential therapeutic effects: anti-cancer, huntington’s disease

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18
Q

DNA base pairing

A

A-T

C-G

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19
Q

RNA base pairing

A

A-U

C-G

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20
Q

Antiparallel structure of DNA

A
  • 5’ end has phosphate group
  • 3’ end has hydroxyl group
  • 2 strands run in opposite directions
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21
Q

DNA helicase

A
  • unwinds/opens double helix

* hydrolyzes ATP

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22
Q

Single strand binding protein (ssBP)

A
  • assiste helicase

* stabilize and straighten single strands of DNA

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23
Q

origin of replication

A
  • specific DNA sequences

* AT rich sequences (A-T has 2 bonds, whereas C-G has 3)

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24
Q

DNA polymerase types

A
  • Prokaryotes: polymerase I -> removes RNA primers, polymerase III -> major DNA polymerase
  • Eukaryotes: alpha, beta, delta, gamma (mitochondria) and epsilon
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25
Q

primers

A
  • required for DNA polymerase to function, but not RNA polymerase
  • formed at the point of initiation of new chain
  • contains RNA, not DNA (also means uracil instead of thymine)
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26
Q

DNA primase

A

makes primers

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27
Q

Directionality of DNA polymerase

A
  • always adds nucleotides to the 3’ end (hydroxyl group)

* in other words, DNA replication occurs in the 5’ to 3’ direction

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28
Q

okazaki fragments

A
  • the lagging strand in DNA synthesis

* oriented 3’ to 5’, meaning that primers have to be added/replication occurs in pieces

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29
Q

Primer removal

A
  • After DNA synthesis complete up to the primer, RNA primer removed and replaced with DNA.
  • EUKARYOTES: DNA polymerase delta
  • prokaryotes: DNA polymerase I
30
Q

DNA ligase

A
  • joins okazaki fragments together in lagging strand

* creates phosphodiester bonds

31
Q

topoisomerase

A
  • prevents DNA tangling

* breaks DNA then reseals to relieve tension/twists

32
Q

topoisomerase I

A

breaks single strands of DNA then reseal

33
Q

topoisomerase II

A

breaks double strands of DNA then reseal

34
Q

quionolone antibiotics

A

inhibits prokaryotic topoisomerase enzymes -> breaks in DNA strands that cannot be resealed

35
Q

chemotherapy agents

A
  • inhibit eukaryotic topoisomerases -> disrupts cells that are rapidly dividing
  • ex etoposide/teniposide, irinotecan/topotecan, anthracyclines
36
Q

semi-conservative nature of DNA replication

A

new DNA = one old and one new strand

37
Q

proofreading of DNA replication

A
  • DNA polymerase can move backwards and correct errors if the wrong base is added
  • it’s called 3’ to 5’ exonuclease activity
38
Q

telomeres

A
  • nucleotides found at the end of chromosomes
  • contain TTAGGG sequences
  • No place for RNA primer on lagging strand
  • problem in eukaryotic cells (non-circular DNA)
39
Q

telomerase

A
  • recognizes telomere sequences
  • adds them to new DNA strands
  • Contains RNA template
  • “RNA-dependent DNA polymerase”
  • avoids loss of genetic material
40
Q

where will you find a lot of telomerase?

A
  • cells that need controlled indefinite replication
  • hematopoietic stem cells
  • epidermis, hair follicles, intestinal mucosa
  • Implicated in many cancers - allows immortality
41
Q

Sources of DNA damage

A

Heat, UV radiation, chemicals, free radicals, etc

42
Q

Depurination

A
  • occurs spontaneously thousands of times/day

* loss of purine bases (G and A)

43
Q

Deamination

A
  • occurs spontaneously hundreds of times/day

* base loses amine group (usually cytosine, which make uracil)

44
Q

Base excision repair

A
  • for single stranded DNA repair
  • recognizes specific base errors (deaminated bases, oxidized bases, open rings)
  • enzymes vary
  • removes damaged base -> removes phosphate backbone -> adds back new nucleotide
  • through all phases of cell cycle
45
Q

DNA glycosylase

A

removes damaged bases

46
Q

AP endonuclease

A
  • recognizes nucleotides w/o base
  • attacks 5’ end
  • nicks damaged DNA upstream of AP site
  • creates 3’-OH end adjacent to AP site
47
Q

Apurinic of apyrimidic nucleotide

A

backbone without the base

48
Q

AP lyase

A
  • some DNA glycosylase also have AP lyase activity

* attacks 3’-OH end of ribose sugar

49
Q

example mechanism of base excision repair

A
  1. glycosylase removes damaged base
  2. AP endonuclease and AP lyase remove the phosphate backbone where the damaged base was removed
  3. DNA polymerase adds back new base
  4. DNA ligase seals the strand
50
Q

nucleotide excision repair basis

A
  • remove damage that involved multiple bases
  • often used to repair pyrimidine dimers caused by UV damage
  • Active in G1 phase (prior to DNA synthesis)
51
Q

mechanism of nucleotide excision repair

A
  • endonucleases remove the damaged bases
  • DNA polymerase adds new bases back
  • DNA ligase seals DNA
52
Q

xeroderma pigmentosum

A
  • results with defective nucleotide excision repair
  • extreme sensitivity to UV rays
  • signs appear in infancy or early childhood
  • dry skin (xeroderma)
  • changes in pigmentation
  • HIGH risk of skin cancer
53
Q

Mismatch repair (MMR)

A
  • incorrectly placed bases (insertions, deletions, incorrect matches) that proofreading missed
  • NO damage to base
  • Occurs in S/G2 phase (after DNA synthesis)
  • newly synthesized strand compared to template strand
  • errors removed then resealed
54
Q

Microsatellite

A
  • repeating segments in DNA

* mismatch repair important for stability of microsatellite

55
Q

DNA slippage

A
  • can occur at repeats of microsatellites
  • results in mismatch
  • repaired by MMR systems -> stable number of repeats
  • can cause insertions/deletions -> frameshift
56
Q

HNPCC = Hereditary Non-Polyposis Colorectal Cancer = lynch syndrome

A
  • germline mutation of DNA mismatch repair enzymes (mostly MLH2 and MSH2 mutations)
  • leads to colon cancer via microsatellite instability**
57
Q

Homologous end joining (HEJ)

A
  • for double stranded DNA damage

* uses sister chromosome as a template

58
Q

non-homologous end joining (NHEJ)

A
  • for double stranded DNA damage
  • uses proteins to re-join broken ends (DNA pol lamba and mu)
  • no template -> highly error prone
59
Q

Fanconi anemia

A
  • inherited aplastic anemia
  • more than 13 gene abnormalities can lead to it; many involve DNA repair enzymes
  • hypersensitivity to DNA damage
  • cells vulnerable to DNA strand cross-links
  • also impaired homologous recombination
60
Q

ataxia telangiectasia

A
  • defective NHEJ
  • mutations in ATM gene on chromosome 11
  • DNA sensitive to ionizing radiation
  • CNS, skin, immune system affected
  • usually 1st year healthy, then slow dev, progressive motor coordination problems
  • high risk of cancer
61
Q

point mutations

A
  • 1 base switched for another
  • transitions (more common)- purine to purine or pyrimidine to pyrimidine
  • transversion - purine to pyrimidine or vice versa
62
Q

silent mutation

A
  • nucleotide substitution codes for same amino acid

* often is a base change in the 3rd position of codon

63
Q

nonsense mutation

A

nucleotide substitution -> early stop codon

64
Q

missense mutation

A

nucleotide substitution -> codes for different amino acid

65
Q

sickle cell anemia cause

A
  • caused by missense mutation in beta globin gene

* adenine changed with thymine -> valine changed to glutamate

66
Q

insertions/deletions

A
  • addition/subtraction of nucleotides

* can alter protein product

67
Q

cystic fibrosis cause

A

deletion of 3 DNA bases -> loss of phenylalanine

68
Q

frameshift mutation

A
  • insertion/deletion (not multiple of 3) that alters reading frame
  • massive change in protein
  • can result in early stop codon or loss of stop codon
69
Q

Histone Deacetylase (HDAC)

A

removes an acetyl group from histones

70
Q

histone acetyltransferase (HAT)

A

add acetyl groups to lysine residues on histones

Molecular Foundations of Medicine (21 decks)

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