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Core I > exam II > Flashcards

exam II Flashcards

1
Q

semiconservative DNA replication

A

when both parent strands attatch to new daughter strands so one of the original is always in each new duplex

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2
Q

deoxynucleotide monophosphates addition to new chain

and what bond

A

dNTP have Ps cleaved by DNA poly when adding to the chain with a phosphodiester bond btwn 3’OH of alast group and 5’P of new one

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3
Q

direction of DNA synthesis

A

built 5’ to 3’ so it reads template 3 to 5

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4
Q

primosome and components

A 
protein complex for finding origin and making primer
DnaA - 
DnaC
DNA helicase (DnaB)
SSB 
DNA primase
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5
Q

leading vs lagging strand

A

leading is when the 3’ end is exposed so it can go toward the unwinding continuously (processive)
laging is when 5’ prime is exposed so needs to make a primer repeatedly and move away chunk by chunk from unwinding site

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6
Q

okazaki fragments

A

the discontinuous sections on the lagging strand with individual primers

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7
Q

replisome and components

A 
found at replication fork for helping polymerase
has similar stuff to primosome but allso
Poly I
DNA ligase
Topoisomerase
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8
Q

bacterial replication

and enzymes

A

starts at oriC moving bidirectionally

uses primosome proteins

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9
Q

eukaryotic DNA polymerase gamma, delta, epsilon

A

gamma - in mitochondria for genome
delta - nuclear lagging elongation and repait
epsilon - nulcear leading elongation and repair

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10
Q

which euk DNA polymerase has primase actiivty

A

alpha has primase activity for initiation

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11
Q

nucleosome

A

only in euk fundamental unit of chromatin packaging containing histones
its the wound up beads

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12
Q

telomers

role of

A

non-coding nucleotide sequence at end of linear chromosomes

has shelterin to protect ends

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13
Q

which strand is elongated by telomerase

A

3’ end is elongated because it adds a new telomere repeat to an RNA template on the telomerase then primer can be bound to new 3’ group to build that strand

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14
Q

RNA component of Telomerase template or primer

A

template for extending 3’ end so that primer can be added and extnd 5’ group before removal

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15
Q

telomerase in somatic cells?

A

no which is why it gets shorter every replicatino possiblity leading to aging

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16
Q

semidiscontinuos replication

A

just the idea of a leading sstrand being continusoul and the lagging strand being discontinuous

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17
Q

origin of replication

A

the oriC in prok found by primosome has lots of AT

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18
Q

replicaiton fork

A

just where strands separate into leading and lagging

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19
Q

primers

A

short RNA bound to dna weakly to help bring DNA poly III in

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20
Q

proof reading

A

3’->5’ exonuclease activitigy removing incorrect base pairs

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21
Q

prok vs euk DNA rep

A

euk has multiple origin sites
more polys
telomerase

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22
Q

DnaA

A

binding protein for oriC short repeats usually of AT
initial melting and brings other proteins
ATP yes

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23
Q

DnaC

A

brings DnaB

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24
Q

DNA helicase

A

is DnaB unwinding duplex

ATP yes

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25
Q

SSB

A

single- stranded DNA binding protein stabalizes single strands

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26
Q

DNA primase

A

DnaG makes RNA primers on DNA for DNA poly

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27
Q

DNA poly I

A

removes RNA primers and fills with DNA

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28
Q

DNA ligase

A

seales nicks between DNA fragments by hydrolyzing ATP

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29
Q

topoisomerase

A

unwind supercoils by breaking and rejoining DNA strands i think makes helicase work

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30
Q

histone

A

positively charged beads forming ionic bonds with negative DNA

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31
Q

examples of DNA damage

A 
UV
oxygin radicals
damination
alyklation
depurination
drugs, metabolism, poly, tobacco
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32
Q

sun damage

A

UV light makes incorrect covalent bonds changing structure making Kink that stops polymerase
thymine (pyrimidine) dimers

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33
Q

oxygen damage

A

reactive oxygen species can alter DNA like changing G to 8-oxoguanine changing behavior to an AT bond instead of GC

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34
Q

DNA mutations

A

gene, chrom, genom

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35
Q

gene mut

A

point

  • bas sub
  • deletion/insertion
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36
Q

chromosomes mut

A

insertion
deletion
translocation

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37
Q

genom mut

A

loss or gain of entire chromosome

like how downs has extra 21 causing trisomy

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38
Q

damage vs mut

A

damage is reversible 1 in 1000 becomes mut

mut is permanent hereditary

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39
Q

mismatch repair of e coli

A

only post DNA replication
MutS is wrapped around backbone sliding until finds distortion from missmath
conformational change brings MutL and MutH
MutL forms a loop
MutH finds methylated GATC and endonuclease makes nick and removes backbone from GATC to after bad base then exonuclease removes bad base
DNA polymerase adds base and ligase seals backbone

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40
Q

base excistion repair

A

any cell cycle stage
modified bases like oxidative damage, deamination, alkylation
DNA glycosylase finds lesion and removes base making AP site
endo and exonuclease remove deoxyr ribose of backbone
DNA polymerase beta and ligase seal nick

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41
Q

BER vs NER

A

free bases vs oligoucleotides
oxidative and alkylation vs UV induced bulky lesions
one cut vs 2 cut excinuclease
aging and cancer vs defieiency

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42
Q

which DNA repair system is error prone

A

only NHEJ

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43
Q

clinical consequences

A

d

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44
Q

HNPCC

A

hereditary non-polyposiss colorectal cancer

casued by microsatelie instablitiy and slipped mispairing and extra loops when MMR messes up

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45
Q

XP

A

xeroderma pigmentosum when XP proteins from NER are inactivated by mutations makes super sensitive to UV damage and cancer

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46
Q

2 main DNA protection strategies

A

damage avoidance - ezymes to nuetralize ROS (superoxide demutase then peroxidase catalase)
melinin releases UV as heat
or the 6 types of repair

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47
Q

Direct reversal of damage

A

no nicking, no recruiting
fixes stuff like pyrimidine dimers which can stop replication
DNA photolyase can recognize in dark but only repair in light
(not in placental mammals)
or O6 methyl guanine
one protein (alkyltransferase) used up to remove one methyl

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48
Q

global nucleotide excision repair

A 
in all organisms, repairs  helix distorting DNA damage
like pyrimidine dimers gets recognized
helicase makes bubble 
2 cuts by excinuclease (XP protein)
polymerase and ligase reclose
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49
Q

homologous recombinatino

A

repairs double strand breaks
copies section from homologous pair then reattatches
happens in S phase so it has chromosome template or G2
RAD 51 mediates pairing

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50
Q

non-homologuous end joining

A

also for double stranded break but during G1 when no sister
end trimmed by exonuclease
DNA-PK
so its trimmed rematched and rejoined ligation

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51
Q

base subst

A 
point
C->T tumors
G->T lung cancer
transition
transversion
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52
Q

transition

A

purines to purine

pyrimidine to pyrimidie

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53
Q

transversion

A

pyrimidine purine

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54
Q

deletions

A

chrom mut

leads to truncation

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55
Q

translocaiton

A

2 non homoloougs exchange chunks becoming chimeric

philly is this for 9 and 22

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56
Q

transcription coupled NER

A

during transcription

protiens from CSB and CSA which if inactivated cause cockayne syndrome

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57
Q

cockayne syndrom

A

developmental arrest and UV sensitivity but not increased risk of cancer

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58
Q

features of transcription

A

not entire genome
specific genes
gene expression restricted to products needed
regulatory sequences mark begin/end and specify template

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59
Q

RNA polymerase vs DNA poly

A

ribo vs deoxy
no primer (less accurate)
different enzymes
absolutely processive

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60
Q

transcriptional unit

A

where RNA poly and factors interact on DNA
promoter - RNA binds and starts, not transcribed, dictates direction
terminator - cis end where RNA poly falls off

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61
Q

key aspects of transcription cycle

A

initiation
elongation
termination

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62
Q

pro vs euk transcr

A

nuclear membrane in Euk separates transcript/lation
pro=polycistronic
euk = monocistronic

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63
Q

general transcription factor functions

A

initiat transcript and bring euk RNA poly to DNA
for RNA polymerase II called TFIIs
interact at core promoter

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64
Q

TF order and effect

A

TBP binds TATA box
TFIIB stabilizes TBP
TFIIF brings RNA poly II and TFIIE which brings TFIIH
TFIIH unwinds DNA

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65
Q

script initiation

A

sigma helps rna poly find promoter sequence
transcription bubble
bonds 2 dNTPs
promoter clearance

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66
Q

script elongation

A

sigma leaves and poly continues until stop site and polymerase release

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67
Q

script termination

A

intrinsic termination when reaches site missing factors and high GC where RNA self binds making loop
isomerization causes hairpin
weakens affinity for DNA

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68
Q

Characteristics of prok gene expression and 3 reg proteins

A 
gene clusters called operons on/off
polycistronic - 1 gene for many RNA
specificity factors - alter spec of RNA poly
repressosrs - impede RNA poly access
activators - enhance access
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69
Q

lac operon

A 
on/off
dual control
negative regulation
depressed state
positive regulation
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70
Q

trp operon

A

5 genes with single promoter
coordinate control
low trp - all genes transcribed
high - repressor binds to trp and blocks RNA polu
drop in Trp - repressor releases Trp starting back up again

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71
Q

mech of euk transcription activation

A

activators and repressors bind near or far from the gene

enhancers help recruit machinery independent of orientation and position

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72
Q

regulation of TF

A 
factor only present in need
factor needs activation
ligand control
stuck in membrane
inhibitory protiens 
needs a buddy (dimeric activity)
phosphorylation
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73
Q

regulation of nuclear steroid/hormone receptors

A

steoid receptor bound to heatshock in cytosol until steroid comes releasing it so it can enter nucleus bind and activate
hormone receptor already in nuc when ligand comes binds and to receptor activating gene - zn finger

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74
Q

E2f regulation

A

cell cycle regulator
G1->S phase
E2f bound to RB protein until kinase CDK phosphorylates RB remiving it so E2f can activate genes to make S phase happen
CDK activated by growth factors

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75
Q

p53

A

TF
‘guardian of the genome’ tumor suppressor
stops cell cycle when DNA damage, if still cant fix kills self (apoptosis)

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76
Q

negative regulation lac

A

only glucose
repressor is bound to operator region
gene off

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77
Q

depressed state lac operon

A

glucose and lactose available
lactose isomer removes repressor
low expression because no CAP at promoter

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78
Q

positive regulation

A 
only lactose
ATP becomes cAMP cuz glucose absetn
cAMP + CAP binds promoter
repressor gone
gene on
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79
Q

attenuation of Trp operon

A

normal mRNA has 1-2 and 3-4 loop (3-4 terminates) ahead of the trp gene
low Trp the ribosome stalls at Trp codon so 2-3 hairpin forms preventing 3-4 so the ribosome can make it to the gene
otherwise trp is present so hits 3-4 and leaves

80
Q

diff btween lac and trp operon

A

when lactose is present repressor is removed so lac gene is active
when trp is present repressor is activeated and gene turns off
makes sense because lac is looking to use extra source while trp is trying not to make too much

81
Q

mechanisms of transcription repression

A 
competitive DNA binding
masking activation surface
direct interaction w/ TF
recruitment of chromatin remodeling complex
recruitment of Histone deacetylases
82
Q

transcription repression competitive DNA binding

A

repressor and activator have overlapping binding sites

83
Q

transcription repression masking activation surface

A

repressor binds to activator when both bound to DNA preventing activators effect

84
Q

transcription repression direct interaction with GTF

A

binds and prevents GTF assembly

85
Q

transcription repression recruitment of chromatin remodeling complex

A

returns it to pre initiation hiding the TATA box

86
Q

transcription repression recruitment of histone deacetylases

A

deacetylases histones so they are positive again and bind tighter

87
Q

dna methylation

A 
added to C of CpG islands
interferes with transcription factors not GC pairing 
readers writers erasers
hyper - no expression
hypo - expression
cuz more blocks TF
88
Q

histone modification

A

reversible, known as histone code
could be phosph-, meth, or acetylation
main one is acetyl

89
Q

readers meth

A

recognize and bind to methyle groups

MECP2, MBD!-4

90
Q

writers - meht

A

add meth to C

DNA methyltransferases DNMT

91
Q

erasers meth

A

modify and remove meth
in active demeth
TET enzyme

92
Q

mechanism of epigenitc regulation and gene expression

A

just meth and acetyl again

93
Q

epigenetic diseases

A

Rett syndrome - mut of MECP2 in X linked so female and means stalled development
cancer

94
Q

pros/cons of epigenetics studies

A

helps link diseases and find cures

cant account for environment

95
Q

long vs short non coding RNA

A

both regulate neighboring genes
long deregulate in disease Tsix, chromatin remodeling
short are like miRNA for biomarkers
long interacts with proteins Xist masks a chromosomes

96
Q

exosomes

A

cell to cell transfer
multi vessicel bodies
bring like proteins and miRNA
also good for biomarkers

97
Q

histone code

A

modifications read by TF akin to a language

98
Q

histone acetylation

A

HAT enzyme
hyper - active
hypo - inactive
more acetylation make more negative so less affinity to DNA so easier for TF to bind

99
Q

writers acetylation

A

HAT

histone acetyl transferase

100
Q

readers histone a

A

bromodomain proteins

101
Q

erasers HA

A

Histone DeAcetylases

102
Q

RNA splicing steps

A

extron intron extron
intron pinched off
spliceosome of snRNAs

103
Q

role of snRNPs in splicing

A

U1 finds splice site
U2 binding branch point
U4-6 change shape acting as spliceosome pinching off section between exons

104
Q

splicing fidelity

A

ordered and coupled with transcriptions so only one set of e-i-e exposed and able to splice at a time
uniform exon length marks start stop

105
Q

5’ end processing of mRNA

elements and time

A

capping
co
decapped post

106
Q

3’ end processing of mRNA

elements and time

A

co
happens as cleavage once AAUAA happens
more built after but then cleaved

107
Q

alternative splicing

A

increases diversity cuz 1 gene many proteins

skipping or includinding different introns and exons

108
Q

mature mRNA between transcription and translation

A

d

109
Q

mRNA features and role in gene expression and RNA metabolism

A

d

110
Q

mRNA degredation

A

rate of poly A tail degredation determines

exosome has enzymes

111
Q

hnRNA

A

heterogenous RNA, includes pre-mRNA

112
Q

pre-mRNA

A

transcript prior to mRNA

113
Q

snoRNA

A

small nucleolar RNAs, help process and modify rRNA

114
Q

snRNP

A

small nuclear RNAs, splicing of pre-mRNA

115
Q

Spliceosome

A 
mediates splicing in EUK
5 snRNPs
interacts with hnRNPs
can be ribosome sized
components added sequentially as sites emerge from RNA poly II
116
Q

tRNA modification and processing

A

RNAase P cleaves 5’
exonuclease cleaves 3’
in nucleolus

117
Q

rRNA modification and processing

A

RNA pol I transcript

done by snoRNPs

118
Q

mRNA

A

messenger, code for proteins

119
Q

rRNA

A

ribosomall, basic structure of ribosome and catalyze protein syn

120
Q

tRNA

A

transfer, adapter btwen RNA and amino acids

121
Q

RNA processinog steps

A 
Capping
splicing
3'polyadenylation
transport
proofreading
122
Q

Capping

A

co-transcriptional

phosphorylation causing 5’-5’ linkage

123
Q

postitive atternative spliing regu

A

add activator

124
Q

negative alternative splicing regu

A

add repressor

125
Q

components of general translation of mRNA to protein

A

amino acids
MRNA template code
tRNA brings aminoacyl-tRNA to ribosome
rRNA nucleic acid, autocatalytic
aminoacyl-tRNA synthetase makes amino acid attatch to tRNA
ribosomes - rRNA + portein making machinery
ATP or GTP

126
Q

stages of protein syn

A 
activation of amino acids
initiation
elongation
termination
recycling
co/post processing
127
Q

direction of ribosome

A

reads mRNA 5’to3’

128
Q

codon

A

3 base pairs signalling amino acid
AUG is start (methionine)
UGA UAA UAG termination/stop/nonsense codons

129
Q

tRNA anticodon to mRNA codon interaction

A

adaptor hypothesis

anti codon binds antiparallel to codon

130
Q

direction of sequential adition of amino acids

A

AA attatched to 3’ end

N to C terminus

131
Q

genetic code

A

order of bases = which AA made
3 bases per aa
universal

132
Q

degeneracy vs lack of ambiguity

A

degen= multiple codons per amino acide

unambiguous - one amino acid per codon

133
Q

wobble hypto

A

third base codon (so first anticodon) much less important so tRNA can bind to more than one codon
A becomes H so not watson crick

134
Q

altering NT sequence changes protein

A

mutations like point can be silent if 3rd changed, missense changes charge not AA if 1st or 2nd nonsense if loses stop codon
frameshift will change codons because read in wrong triplets

135
Q

protein syn stage in cytoplasm

A

activation

136
Q

protein syn stage in ribosome

A

initiation
elongation
termination
recycling

137
Q

overall structure of tRNA

A

cloverleaf 2D
3’CCA attaches to amino acid
anticodon binds to codon

138
Q

modified bases of tRNA

A

idk but they change structure

139
Q

formation of aminoacyl-tRNA

A

performed by aminoacyl-tRNA synthestase

1. ATP~AA=AA-AMP~2tRNA=AA-tRNA

140
Q

function of aminoacyl-tRNA

A

protects AA on way to ribosome

141
Q

sedimentation coefficients prok

A

30+50=70

16s

142
Q

sedimentation coef euk

A

60+40=80
small for decoding and fideltiy
large for peptidyl transferases

143
Q

translation initiation

A

Energy yes
mRNA~small ribosome+aminoacyl-tRNA brings ribosome
eIF1,2

144
Q

translation elongation

A

energy yes
polypeptide chain formed
guanine exchange factor removes GTP and reactivates EF to restart cycle
ribosomal peptidyl transferase is ribozyme forming pepide bond

145
Q

translation termination

A

eRF1 finds stop codon and binds with eRF2-GTP to hydrolyze peptide chain

146
Q

translation recycling

A

ribosomal complex, factors and tRNA release to be reuased

147
Q

euk vs prok translation

A

prok dont scan mRNA to find AUG
no ATP
just finds SD sequence
coupled with transcription

148
Q

SD sequence

A

shine-delgarno purine rich sequence that prok finds to line up with AUG instead of scanning for AUG

149
Q

21st AA

A

selenocysteine

150
Q

22 AA

A

pyrolysine

151
Q

selocysteine generation

A

recognized by same aminoacyl-tRNA as serine

knocks of OH oh selenium and becomes selenocysteine

152
Q

UGA involvement of selenocysteine and selenoprotein

A

mRNA reaches UGA but 3’ non coding region SECIS structure recognized with protein and then EF so it sees UGA as selenocysteine codon and reaches other stop codon

153
Q

pioneering round of mRNA translation

A

first round when EJC is there and makes upstream stop codon

154
Q

non-stop-mediated mRNA decay

A

decay when lack of stop codon

155
Q

defects related to no-go/stop decay

A

go-

stop-

156
Q

nonsense-mediated decay

A

mRNA with premature termination

UPF, SMG

157
Q

nonsense-mediated decay

A

mRNA with premature termination
UPF, SMG
EJC make earlier stop codon activity

158
Q

nonsense decay related defect

A

same things that helped discover UPF and SMG

159
Q

SMG

A

suppressorm with morphenaginic defect on genetailia

160
Q

EJC

A

exon junction complelx

161
Q

EJC

A

exon junction complex

162
Q

phosphorylation of eIF2

A

affects levels of eIF2-GTP in response to stress
kinases add P
blocks release of GDP so GTP cant reparticipate in initiation
locks eIF2B in place eIF2b causes GDP release so its stuck not releasing anywhere else either

163
Q

mTOR regulation

A 
mechanistic target of rapamycin
mTORc1 activated by good things (AA, ENERGY, etc) for cell, inhibited by bad things 
mTORC2 just activated by growth factors 
activated by non stress
inhibited by stress
164
Q

how mTOR globally regulates

A

mRNA translation, ribosome biogenesis, autophagy, metabolism
mTORC turned on by good things and turns on good things like growth
turns off 4E-BP which inhibits eif-4e
so mTOR turns on eif4e

165
Q

cystolic polyadenylation

A 
CPElement
CPE-binding protein
in cytosol 
on an mRNA recruits other factors 
PARN limits PolyA tail
add P and tail grows
166
Q

cystolic polyadenylation control of translation

A

CPEB gets P
other factors open up
poly AA extended so eiF4E can come and be initiated

167
Q

subcellular targetting and translation

A

mRNA brought to specific cell regions by factors
translation localized
BDNF

168
Q

ferritin

A

it stores Fe so wants to be active when Fe is high
IRE-BP bond to IRE when Fe is low blocking coding region
but IREBP do not bond when Fe is high so ferritiin region is accessible.

169
Q

transferritin

A

it brings Fe into the cell so when FE is low we want more of it
IRE-BP binds to IRE when Fe is low preventing degredation of mRNA
IRE-BP does not bind when it is high allowing degradation

170
Q

phosphorylation of eIF2

A

high stress = high eIF2alpha-P, low eIF2-GTP
delayed re-initiation so ATF 4 produced in stress because it takes longer for small 40 s ribosomal subunit to find eIF2GTP so it finds at a later AUG on mRNA

171
Q

IRES

A

internal ribosome entry sites

secondary loop that directuly recruits factors without 5’ cap

172
Q

AA levels affect mRNA translation

A

low slow ribosome
speed affects folding
fast prevents aggregation
slow allows coordinated folding

173
Q

tRNA levels affect mRNA translation

A

low slow ribosome

174
Q

rare codon use affect mRNA translation

A

high slow ribosome

175
Q

how antibiotics target translation and inhibit mRNA

A

resemble aminoacyl-tRNA and bind to A sight of ribosome causing premature termination euk and prok
inhibit peptidyle transferases prevent elongation in euk
bind to 30s subunit prevent fmet-tRNA preventing initiation prok

176
Q

pro vs euk antiboiotics

A

different subunits bound and stages stopped

know the prok and euk subunits

177
Q

origin and function of siRNA in plants and lower euk

A

short interfering RNAs
from Dicer cleaaege of longer dsRNAs
RNA interference is its sliencing
degrades with RISC

178
Q

origin and function of miRNA in vertebrates

A 
microRNA
processed form RNA Pol II transcripts
same length as siRNAs
incomplete complementary
has own RISC
179
Q

biosynthetic pathway of miRNA

A

RNA pol II transcript makes primary-miRNA
Drosha/DGCR8 microproccessor cuts into pre-miRNA w/ 3’ overhang
exportin sees 3’ brings to cytoplasm
DICER cuts off terminal loop aided by TRBP and recruites ago making RISC

180
Q

RNA silencing

A

gene suppression oby small RNAs

transcript and post transcript

181
Q

RNA processing into miRNA?

A

same as biosynthetic pathway

182
Q

model for miRNA post-translation gene reg in vertebrates

A

d

183
Q

determinants of miRNA binding to a target mRNA

A

d

184
Q

factors affecting streght of silencign by miRNA

A

d

185
Q

global regulation of miRNA

A

d

186
Q

selective regulation of miRNA

A

d

187
Q

miRNA alter expression of target genes

A

d

188
Q

miRNA biomarkers for disease

A

d

189
Q

miRNA therapy for disease

A

d

190
Q

what and where CRISPR-Cas

A

d

191
Q

origin and function of elements in CRISPR-Cas

A

d

192
Q

3 phases of CRISPR-Cas

A

d

193
Q

target recognition and degradation employed by Type II CRISPR-Cas

A

d

194
Q

dicer

A

endonuclease from RNase III
cuts up dsRNA into siRNAs
leave 2 nt overhang of 3’end, recognized end then cuts certain length repeat

195
Q

RISC

A

siRNA+Argonaute
both bind to mRNA
Ago slices RNA and degrades it

196
Q

dsDNA origin

A

lots but mainly virus

Core I (6 decks)

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