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MBG 2040 > FINAL EXAM FLASHCARDS > Flashcards

FINAL EXAM FLASHCARDS

1
Q

who discovered the DNA double helix structure?

A

rosalind franklin & maurice wilkins

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2
Q

who published the DNA secondary structure?

A

watson & crick

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3
Q

what is DNA’s secondary structure?

A
  • complementary base pairs
  • complementary and anti-parallel strands
  • 10 bp/turn
  • 0.34 nm between stacked bases & 3.4 nm/turn
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4
Q

what does DNA being semi-conservative mean?

A

that the strands separate to regenerate new DNA using the separated strands as a template

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5
Q

what are the 3 ways DNA can split?

A
  • conservatively
  • dispersively
  • semi-conservatively
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6
Q

who discovered that DNA replication was semi-conservative?

A

meselson & stahl using their CsCl density gradient

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7
Q

what are the modes of DNA replication?

A
  • theta replication
  • rolling circle replication
  • linear chromosomal replication
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8
Q

what is theta replication?

A
  • occurs in prokaryotes circular DNA
  • looks like theta before it splits into 2 circular DNA molecules
  • BIDIRECTIONAL
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9
Q

what is rolling circle replication?

A
  • specialized (occurs in F factor & some viruses)
  • produces multiple circular DNA molecules
  • UNIDIRECTIONAL
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10
Q

what is linear chromosome replication?

A
  • occurs in eukaryotes
  • chromosome has many origins which all form replication bubbles until they meet up (producing 2 linear DNA molecules)
  • BIDIRECTIONAL
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11
Q

what does DNA replication require?

A
  • Mg 2+
  • DNa polymerase
  • A, G, C, T
  • template DNA
  • RNA primer
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12
Q

what do RNA primers do?

A

provide the 3’ OH end to initiate DNA synthesis by DNA polymerase

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13
Q

what end of a replicating DNA does nucleotides get added to?

A

3’ end of the new (synthesizing) strand

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14
Q

what are DNA chains susceptible to?

A

DNA chains are susceptible to nuclease cleavage (results in phosphate group staying attached to 5’ carbon or the 3’ carbon

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15
Q

which DNA polymerases are replicative?

A

DNA polymerase 1 & 3

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16
Q

which DNA polymerases are for repairing?

A

DNA polymerases 2, 4, 5

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17
Q

what does DNA polymerase 1 do?

A

removes RNA primers on lagging strand

  • 5’ to 3’ polymerase/exonuclease activity (removal of RNA primers)
  • 3’ to 5’ exonuclease (proofreading)
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18
Q

what does DNA polymerase 3 do?

A

main replicative polymerase

  • 5’ to 3’ polymerase activity
  • cant remove RNA primers
  • 3’ to 5’ exonuclease activity (proofreading)
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19
Q

what is the beta clamp?

A

attaches to DNA and helps keep DNA polymerase 3 on the strand

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20
Q

what is the name of the synthesis of DNA on the lagging strand?

A

discontinuous synthesis (due to okazaki fragments)

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21
Q

what is the name of the synthesis of DNA on the leading strand?

A

continuous (no okazaki fragments)

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22
Q

why is RNA more reactive than DNA?

A

because it has an OH group (not just H) on carbon 2 of ribose

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23
Q

what is the tertiary structure of RNA?

A

tRNAs

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24
Q

how are genes expressed in prokaryotes?

A
  • transcription & translation are coupled (happen in same place)
  • coding region is continuous
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25
Q

how are genes expressed in eukaryotes?

A
  • coding region is non-continuous (contains introns & exons)
  • transcription = nucleus
  • translation = cytoplasm
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26
Q

how is RNA synthesized?

A

using the 3’ to 5’ DNA template strand (nucleotides are added to 3’ end of RNA strand)

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27
Q

what are the differences between DNA replication and RNA synthesis?

A
  • RNA only uses 1 strand to synthesize
  • no primer needed for RNA synthesis
  • uses A, G, U, C instead of A, G, T, C
  • RNA is complementary to DNA template and identical to DNA non-template
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28
Q

what is the -35 sequence (for prokaryotic transcription)?

A

5’ TTGACA 3’ (on non-template strand)

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29
Q

what is the -10 sequence (for prokaryotic transcription)?

A

5’ TATAAT 3’ (on template strand)

- aka. TATA box

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30
Q

where does prokaryotic transcription actually start on DNA?

A

5-9 base pairs down from the -10 sequence (either T or C)

- this is aka. the +1 site

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31
Q

how many base pairs apart are the -35 and -10 sequences?

A

approx. 16-19 base pairs

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32
Q

what is upstream and downstream?

A
  • upstream = anything before the +1 site (actual start of transcription)
  • downstream = anything after the +1 site
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33
Q

what 3 RNA polymerases do eukaryotes have?

A

RNA polymerase 1, 2 and 3

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34
Q

what does RNA polymerase 1 do?

A

transcribes large rRNAs (structural/catalytic components of ribosomes)

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35
Q

what does RNA polymerase 2 do?

A

transcribes pre-mRNA, snRNAs (spliceosomes & tRNA/rRNA modification) and miRNAs (block complementary mRNA expression)

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36
Q

what does RNA polymerase 3 do?

A

transcribes tRNA, small rRNAs, certain snRNAs and miRNAs

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37
Q

where is the TATA box in eukaryotic transcription for RNA polymerase 2, and why?

A

at -25 sequence (because TFIIB recognition site is at -35)

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38
Q

what does the RNA polymerase 2 promoter consist of?

A

regulatory promoter (before -35) and core promoter (-35 to +30 - core promoter element)

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39
Q

who discovered RNA polymerase 2 structure/function?

A

Roger Kornberg

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40
Q

what is the inhibitor of RNA polymerase 2 called?

A

alpha amanitin (inhibits at both initiation & elongation)

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41
Q

what are the 3 main steps of transcription for both prokaryotes and eukaryotes?

A
  1. initiation
  2. elongation
  3. termination
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42
Q

due to prokaryotes continuous coding region, how does that affect the mRNA/protein generated?

A

(amino acids —–> codons on mRNA —–> genes on DNA)
transcription translation

  • no additional processing steps are required to form mRNA
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43
Q

what is the mRNA sequence that is only in prokaryotes?

A

the shine-dalgarno sequence = 5’ UAAGGAGGU 3’

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44
Q

due to introns & exons in eukaryotes, how does that affect the mRNA/protein generated?

A

removal of introns (by RNA splicing) & additional RNA processing steps required to form mRNA

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45
Q

what are exons and introns?

A
  • exons = protein coding segments

- introns = non-coding segments

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46
Q

what are the 3 eukaryotic pre-mRNA processing steps?

A
  1. addition of 5’ cap
  2. addition of 3’ poly A tail
  3. removal of introns
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47
Q

what is a spliceosome made of?

A

snRNPs U1, U2, U4/6 and U5

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48
Q

what is the 5’ splice site on an intron?

A

“GU”

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49
Q

what is the branch site on an intron?

A

a single “A” in middle of intron

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50
Q

what is the 3’ splice site on an intron?

A

“AG”

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51
Q

what is lariat formation?

A

linkage between the 5’ phosphate of “G” (in 5’ splice site) and the 2’ OH of the “A” (branch site)

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52
Q

how can one gene code for many proteins?

A

different modes of splicing and multiple intron 3’ cleavage sites produces different mRNAs from a single pre-mRNA

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53
Q

what are 3 types of RNA editing?

A
  1. changing structures of individual bases
  2. modification of mRNA by guide RNAs
    - guide RNA adds nucleotides to mRNA that weren’t encoded by DNA
  3. insertion or deletion of uridine monophosphates
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54
Q

what is the function of tRNAs?

A

carries the anti-codon for the mRNA’s codon, and the respective amino acid (attached to it’s 3’ end - ALWAYS ACC)

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55
Q

what is the function of rRNAs?

A
  • key component of the ribosome (composed of large and small subunit)
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56
Q

what is the function of the ribosome?

A

RNA machine that forms peptide bonds between amino acids in protein synthesis

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57
Q

where does rRNA synthesis occur in eukaryotes and prokaryotes?

A
  • eukaryotes = nucleolus

- prokaryotes = has no nucleolus, so in cytoplasm

58
Q

what are the eukaryotic ribosome subunits?

A

60S (large) subunit + 40S (small) subunit = 80S ribosome

59
Q

what are the prokaryotic ribosome subunits?

A

50S (large) subunit + 30S (small) subunit = 70S ribosome

60
Q

who discovered “one gene, one colinear polypeptide”?

A

beadle & tatum

- yanofsky discovered that nucleotide triplets corresponded to amino acid sequence in a protein

61
Q

why is the genetic code a triplet code?

A

because 4 bases ^ (3 codons) = 64 (more than enough to encode all amino acids)
- single and double codons = 4 and 16 (not enough for 20 amino acids)

62
Q

who discovered that the genetic code is triplet?

A

crick & colleagues (generated “crick’s wobble hypothesis”)

63
Q

what feature of the triplet code explains degeneracy?(more than 1 codon for an amino acid)

A

the 3rd codon position is a “wobble” codon

64
Q

what is crick’s wobble hypothesis?

A

that base pairing only really occurs between the first 2 codons

65
Q

how does the amino acid get linked to the tRNA?

A

using the aminoacyl tRNA synthetase (there is one for each amino acid, therefore 20)

66
Q

what are the 3 main steps in prokaryotic & eukaryotic translation (protein synthesis)?

A
  1. initiation
  2. elongation
  3. termination
67
Q

what are the 3 sites in the ribosome?

A 
A = aminoacyl site (tRNA binds to mRNA)
P = peptidyl site (formation of peptide bonds between AA) 
E = exit site (where empty tRNA leaves)
68
Q

how does the aminoacyl tRNA synthetase work?

A
  1. AA reacts w/ ATP, producing AMP + PPi (AMP binds to COO- on AA)
  2. tRNA binds to COO- of amino acid kicking off AMP
69
Q

who discovered the ribosome structure & how it operates during protein synthesis?

A

ramakrisham, steitz and yonath

70
Q

what is quality control of RNA and proteins?

A

eliminating mRNAs with errors

71
Q

what are the 3 types of eliminations of mRNAs (for quality control of RNA/proteins)?

A
  1. mRNAs with nonsense mutations
  2. mRNAs where ribosome can’t complete translation
  3. chemically damaged mRNAs
72
Q

what are the types of mutations?

A
  • point mutations (base substitutions, frameshift mutations, and tautomeric shifts)
  • expanding nucleotide repeats
73
Q

what is a pyrimidine?

A

T & C

74
Q

what is a purine?

A

A & G

75
Q

what are the base substitutions?

A
  1. transition = pyrimidine to pyrimidine OR purine to purine

2. transversion = pyrimidine to purine (vice versa)

76
Q

how many base substitutions are there?

A

12

77
Q

what is a frameshift mutation?

A

inserting/deleting ONLY 1 or 2 base pairs (alters entire reading frame downstream of mutation)

78
Q

what is a tautomeric shift?

A

movement of H atoms from one position on a purine/pyrimidine to another
- generates rare AC and GT base pairing

79
Q

what are expanding nucleotide repeats?

A
  • dynamic mutation caused by errors in replication

- repeating triplet codons causes part of strand to be replicated twice

80
Q

what is a forward mutation?

A

changes wild-type phenotype to mutant

81
Q

what is a reverse mutation?

A

changes a mutation back to wild-type phenotype

82
Q

what is a missense mutation?

A

base substitution = amino acid changes

83
Q

what is a nonsense mutation?

A

base substitution = amino acid changes to stop codon

84
Q

what is a silent mutation?

A

base substitution = amino acid unaffected

85
Q

what is a neutral mutation?

A

missense where AA change has no effect on protein

86
Q

what is a loss of function mutation?

A

mutation that causes complete/partial loss of normal protein function

87
Q

what is a gain of function mutation?

A

mutation that produces a protein that isn’t normally present

88
Q

what is a conditional mutation?

A

only produced under certain conditions (ex. temp)

89
Q

what is a lethal mutation?

A

mutation that results in premature cell death

90
Q

what is a suppressor mutation?

A

second site mutation in a gene that hides or restores a first mutation back to normal (ex. amino acid changes, but is then restored)

91
Q

what are the 2 types of suppressor mutations?

A
  1. intragenic = in same gene

2. intergenic = in separate genes

92
Q

what are the rates for spontaneous gene mutations? (hint: they’re infrequent)

A
  • prokaryotes = 10^-8 to 10^-10 per nucleotide pair/generation
  • eukaryotes = 10^-7 to 10^-9 per nucleotide pair/generation
93
Q

what factors can mutations come from?

A
  • internal factors = spontaneous

- external factors = induced (ex. radiation/chemicals)

94
Q

how is DNA usually damaged?

A

by internal factors such as hydrolysis, oxidation, or alkylation

95
Q

in what ways does spontaneous DNA damage occur?

A
  1. DNA replication errors
  2. DNA replication pausing
  3. endogenous chemical reactions
96
Q

what are examples of DNA replication errors?

A
  • tautomeric shifts
  • transition mutations induced by wobbling
  • strand slippage in repeated sequences
97
Q

what are examples of DNA replication pausing?

A

stalling at a nick (due to ROS, etc)

98
Q

what are examples of endogenous chemical reactions?

A
  • depurination = loss of purine through hydrolysis (leaves AP site - can lead to transition/transversion mutations)
  • deamination = loss of NH2 (cause transition mutations)
  • oxidation = ROS damage to DNA (causes transversion mutations)
  • alkylation = adds methyl groups to bases (causes transition mutations)
99
Q

who discovered induced mutations (DNA damage)?

A

hermann muller discovered you can induce mutations in fruit flies using x-rays

100
Q

what are the chemical agents that can induce mutations in ALL DNA?

A
  • alkylating agents
  • nitrous acid
  • hydroxylamine
101
Q

how do alkylating agents induce mutations?

A

add methyl/ethyl groups to DNA bases (can cause transition, transversion, frameshift, and chromosomal mutations)
- examples = mustard gas, EMS, EES

102
Q

how does nitrous acid induce mutations?

A

removes NH2 groups from the bases A, G, and C (causes transition mutations)

103
Q

how does hydroxylamine induce mutations?

A

adds OH group to C causing it to pair with A (transition mutation)

104
Q

what are the chemicals that can induce mutations in ONLY replicating DNA?

A
  • base analogs = 5-BU, resembles T & 2-AP, resembles A/G (causes transition mutations)
  • acridine dyes = causes frameshift mutations during DNA replication by inserting in between DNA bases (ex. proflavin or acridine orange)
105
Q

what are the mutations induced by radiation?

A
  • UV causes thymine dimers to form (blocks DNA replication & causes DNA breaks)
  • Xray induces mutations through ionization (causes nicks & double strand breaks)
106
Q

what are the 6 DNA repair mechanisms?

A
  1. direct reversal of DNA damage
  2. base excision repair
  3. nucleotide excision repair
  4. mismatch repair
  5. recombination
  6. translesion DNA polymerases
107
Q

what is direct reversal of DNA damage?

A
  • direct repair of thymine dimers by photolyase (only in prokaryotes)
  • enzymes removing alkyl groups from DNA bases
  • repairing nicks in DNA with ligase
108
Q

what does base excision repair do?

A

specifically recognizes & repairs damaged DNA bases (found in prokaryotes & eukaryotes)

109
Q

what does nucleotide excision repair do?

A

removes thymine dimers (entire strand & re-synthesizes) and bulky DNA damage

110
Q

what does mismatch repair do?

A

recognizes mismatched bases in new strand by identifying hemi-methylated GATC sequence
- defects in mismatch repair results mutation accumulation

111
Q

what does recombination do?

A

repairs spontaneous/induced double strand breaks

  • homologous = occurs after DNA replication (damaged sister chromatid can be fixed by the other)
  • non-homologous = uses proteins to repair double strand breaks
112
Q

what do translesion DNA polymerases do?

A

replicate through DNA damage (bypassing lesion) so normal replication can occur
- error prone

113
Q

what are transposable elements?

A
  • jumping genes (40% of human genome)
  • major source of mutations
  • can carry antibiotic resistance genes
114
Q

what are the 3 types of transposable elements?

A
  1. cut and paste
  2. replicative transposons
  3. retrotransposons
115
Q

what are cut and paste transposons?

A
  1. IS elements

2. composite transposons

116
Q

what are IS elements composed of?

A
  • gene that encodes a transposase
  • terminal inverted repeats (at both ends)
  • target site duplication (after repeats, at both ends)
117
Q

how do IS elements work as cut and paste transposons?

A
  1. staggered cuts are made in DNA so that a transposable element can insert itself
  2. due to staggered cuts, the gaps filled in by DNA pol. create direct repeats
  • can mobilize anti-biotic resistant DNA during homologous recombination
118
Q

how do composite transposons work?

A

created when 2 IS elements near each other (separated by a gene) trap a segment of anti-biotic resistant DNA

119
Q

what is an example of replicative transposons (hint: found in bacteria)?

A

Ex. Tn3 which can carry anti-biotic resistant genes

  1. Tn3 is replicated to form co-integrate structure
  2. recombination of co-integrate structure separates into 2 separate DNAs (each with a copy of Tn3)
120
Q

who discovered transposons?

A

Barbara McClintock when studying chromosome breakage in corn (discovered cut and paste Ds and Ac transposable elements)

121
Q

what are retroviruses & retrotransposons?

A

use reverse transcriptase to copy retroviral RNA into DNA

- ex. of retrovirus = HIV/AIDS

122
Q

what are retroviruses made of?

A
  • gene that encodes reverse transcriptase/integrase (copies RNA into DNA)
  • terminal inverted repeats & target site duplication
123
Q

what are retrotransposons made of?

A
  • gene that encodes reverse transcriptase/endonuclease
  • contains poly A tail
  • has no terminal inverted repeats
124
Q

what is a long interspersed nuclear element (LINE) made of?

A

ex. L1 element
- contains promoter, 2 reading frames (one encodes nucleic acid binding protein, other encodes protein with endonuclease/reverse transcriptase)

125
Q

what is a short interspersed nuclear element (SINE)?

A
  • only the Alu element can move around
  • do not encode proteins
  • reverse transcriptase required is provided by a LINE
126
Q

what are the major transposable elements in humans?

A

LINEs and SINEs account for 33% of transposons in genome

127
Q

what are the minor transposable elements in humans?

A
  • defective retroviruses

- cut and paste transposon related elements

128
Q

what are the genetic/evolutionary significances of transposons?

A
  1. they’re mutagens
  2. they can mobilize foreign genes (ex. anti-biotic resistant genes)
  3. they can change genome organization
129
Q

what are the 3 types of changes in genome organization (homologous recombination) by transposons?

A
  1. transposable elements in same direction will form a loop when crossing over = deletion
  2. transposable elements in opposite direction will form a bend = inversion
  3. unequal exchange between transposable elements = one chromosome has a deletion, other chromosome has a duplication
130
Q

what is an example of an induced gene?

A

when lactose is present & glucose is absent, gene expression for lac operon is induced (enzymes involved in breakdown are often inducible)

131
Q

what is an example of a repressed gene?

A

when tryptophan is present, genes that make tryptophan are repressed

132
Q

what does an operon consist of?

A

promoter, operator, and series of structural genes

- also a regulator protein, which helps control gene expression

133
Q

what is a negative inducible operon?

A

the lac operon

  • no lactose = regulator protein is active and is able to bind to operator to stop transcription
  • lactose = regulator protein is inactivated by lactose and is unable to bind to operator (transcription occurs)
134
Q

what is a negative repressible operon?

A

the trp operon

  • no tryptophan = regulator protein is inactive and is unable to bind to operator (transcription occurs)
  • tryptophan = regulator protein is activated by tryptophan and binds to operator to stop transcription
135
Q

what is positive control of gene expression?

A

an “activator” - type of regulatory protein (binds to DNA to assist RNA polymerase with transcription)

136
Q

when are the lac operon genes expressed?

A

ONLY when lactose is present, and glucose is ABSENT

137
Q

who discovered the lac operon of E. coli?

A

jacob & monod

138
Q

how does the lac operon have ON and OFF characteristics?

A
  • ON in the presence of allolactose (lac repressor is inactivated by allolactose so transcription of Z, Y, and A genes occurs)
  • OFF in the absence of allolactose (lac repressor is active because no allolactose so it binds to lac operator, halting transcription of Z, Y, and A genes)
139
Q

what are the main mutations in the lac operon? (hint: constitutive expression)

A

I- or Oc results in Z, Y, and A genes always being transcribed (constitutive expression) because I- can’t bind to operator and Oc blocks repressor from binding (I gene)

  • Oc only works if its connected in cis
  • I+ is dominant to I-
140
Q

what are other mutations in lac operon? (hint: no transcription)

A
  • lacIs = lacI repressor always bound to operator (no transcription)
  • lac P mutation = RNA polymerase can’t bind (no transcription)
141
Q

how does the cAMP/CAP complex (regulated by glucose) regulate the lac operon?

A
  • high glucose = low cAMP (cAMP/CAP complex not formed = no binding to lac promoter, no promotion of RNA polymerase binding - no transcription)
  • low glucose = high cAMP (cAMP/CAP complex formed = binding to lac promoter, promotion of RNA polymerase binding - transcription occurs)
142
Q

why is cAMP/CAP complex formed or not formed at certain glucose levels?

A
  • cAMP/CAP not formed when glucose is high because it has sufficient glucose (doesn’t need to produce enzymes to break down lactose)
  • cAMP/CAP formed when glucose is low because it doesn’t have sufficient glucose (needs to produce enzymes to break down lactose for energy)

MBG 2040 (1 decks)

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