Genetics Exam 2

Front 1

Serine

Back 1

OH

Front 2

Threonine

Back 2

OH

Front 3

Arginine

Back 3

Positive, basic

Front 4

Histidine

Back 4

Positive, basic

Front 5

Lysine

Back 5

Positive, basic

Front 6

Glutamine

Back 6

Polar amide

Front 7

Asparagine

Back 7

Polar amide

Front 8

Glutamic acid

Back 8

Negative, acid

Front 9

Aspartic acid

Back 9

Negative, acid

Front 10

IF1 and IF3

Back 10

start formation of translation initiation complex

Front 11

IF3

Back 11

attracts initiator tRNA, then hydrolyzes its GTP to leave so 50S subunit can bind

Front 12

RF1

Back 12

UAA
UAG

Front 13

RF2

Back 13

UAA
UGA

Front 14

RF3

Back 14

binds GTP, helps terminate

Front 15

eRF

Back 15

recognizes all stop codons in eukaryotes

Front 16

Kozaks' rules are:

Back 16

purine _ _ AUGG

Front 17

eIF4

Back 17

recognizes 5' cap
associates with poly-A binding protein during coupling

Front 18

sorting signal

Back 18

amino acid sequence read by sorting proteins, more complicated in eukaryotes

Front 19

polycistronic mRNA

Back 19

coding sequences for more than one protein

Front 20

lac repressor

(and kind of dimerization?)

Back 20

lacI
binds lacO operator
unless inducer allolactose inactivates it

tetramer

Front 21

genes in lac operon

Back 21

lacZ
lacY
lacA

Front 22

lactose and glucose

Back 22

basal transcription of lac operon
no repressor
no enhancer

Front 23

lactose, no glucose

Back 23

high transcription
no repressor
yes enhancer

Front 24

glucose, no lactose

Back 24

low transcription
repressor
no enhancer

Front 25

no lactose, no glucose

Back 25

low transcription
repressor
enhancer

Front 26

catabolite repression

Back 26

glucose indirectly represses lac operon

Front 27

arabinose repressor/activator

Back 27

araC

Front 28

when no arabinose, araC binds to _______

Back 28

2 at araO1
one each at araI and araO2 to connect them in a loop

Front 29

when arabinose is around, araC binds to _______

Back 29

2 at araI--dimer activates transcription
still 1 at araO2, but no loop anymore
still 2 at araO1

Front 30

trp repressor

Back 30

trpR
needs trp corepressor (2 of them) to bind operator

Front 31

trpL

Back 31

leader peptide, attenuator

Front 32

in bacteria, ways of translation regulation are _______

Back 32

- block Shine-Dalgarno
- make secondary structure close to or involving Shine-Dalgarno
- antisense RNA

Front 33

ompF

Back 33

translational regulation: inhibited by micF RNA by complementary binding.
micF produced at high osmolarity because ompF is needed at low osmolarity

Front 34

in bacteria, ways of post-translational regulation are ________

Back 34

- feedback inhibition (protein-protein)
- permanent modifications: proteolytic processing, attaching sugars, lipids, etc.
- temporary modifications: acetylation, methylation, phosphorylation

Front 35

riboswitches are what type of regulation?

Back 35

- translation
or
- transcriptional termination

Front 36

TPP

Back 36

at high concentration, TPP is effector causing riboswitch attenuation for thi operon (responsible for synthesis of TPP)
- also causes blocking of Shine-Dalgarno

Front 37

how do eukaryotic regulatory transcription factors exert their effects?

Back 37

- directly with TFIID
- through coactivator with TFIID
- through mediator with RNA polymerase
- recruiting factors affecting nucleosome composition, DNA compaction

Front 38

euk regulatory transcription factors fight

Back 38

- compete for overlapping enhancers and silencers
- bind each other = masking
- DNA secondary structure = when one binds another can't reach

Front 39

ATP-dependent chromatin remodeling

Back 39

- change nucleosome spacing
- histone eviction
- replacement with variant histones

Front 40

SWI/SNF
ISWI
INO80
MI-2

Back 40

families of chromatin remodelers in eukaryotes

Front 41

ChIP steps

Back 41

- crosslinker
- lysis and micrococcal nuclease
- anti-histone antibody on beads
- spin, take pellet
- break crosslinks
- gel
- add linkers
- PCR with linker primers
- sequence

Front 42

methylation of DNA exerts its effects through _______

Back 42

- methyl-CpG-binding protein works by recruiting HDACs
- methyls block activators from binding to DNA

Front 43

de novo methylation

Back 43

completely new methylation, NOT hemimethylated into fully methylated

Front 44

hemimethylation into full methylation is done by the protein

Back 44

methyl transferase

Front 45

how do insulators exert their effects?

Back 45

- proteins bind to insulator sequences to block enhancer and chromatin remodeling effects of neighboring genes

Front 46

what was that insulator loop and how was it different in males and females?

Back 46

- females: no methylation of insulator, so proteins are bound to insulator, and enhancer has no effect

- males: methylation of insulator makes proteins come off insulators, so the enhancer does have an effect

Front 47

Glucocorticoid mechanism

Back 47

steroid binds to glucocorticoid receptor, heat shock proteins fall off, nuclear localization site exposed, homodimer formed, binds GRE

Front 48

CREB

Back 48

signaling molecule binds receptor activates G protein activates adenylyl cyclase makes cAMP activates protein kinase A phosphorylates CREB that is already bound to CRE, allowing CREB to activate transcription

Front 49

how many of our genes are alternatively spliced?

Back 49

about 70%

Front 50

RNA editing: converting 1 base to another
examples?

Back 50

C to U
A to Inosine (recognized as G)

Front 51

proteins involved in RNA interference?

Back 51

Dicer
RISC complex to attack mRNA
RITS complex to bind mRNA as it is transcribed and recruit histone modifiers to compact that region of DNA
(eg: histone or DNA methylation)

Front 52

example of regulation through affecting translational initiation factors

Back 52

eIF2α is phosphorylated by eIF2α protein kinase (active in emergency conditions), making it form a heterodimer with eIF2B, inactivating eIF2B as an initiation factor

Front 53

the protein that shortens the poly-A tail is called _____

Back 53

deadenylase
has to compete with string of poly-A binding proteins and initiation factors

Front 54

IRP

Back 54

stabilizes mRNA for transferrin receptor (by binding 3' UTR) and blocks 5' UTR for ferritin (both have IRE where IRP binds)

inactivated by iron

Front 55

how to calculate mutation rate?

Back 55

# of new mutations in a gene
_______________________
# of copies of that gene (multiply population size by two for diploid)

Front 56

what are three types of spontaneous mutations and which is the most common?

Back 56

depurination (most common)
deamination
tautomeric shift

Front 57

deamination changes DNA how?

Back 57

C into U (usually caught by base excision repair)
5-methyl C into T

transition, only affects a C

Front 58

tautomeric shift changes DNA how?

Back 58

makes A-C and G-T base pairs

transition

Front 59

how do TNREs get either shorter or longer?

Back 59

DNA pol slips after copying the TNRE, the new strand of which stem loops, and DNA pol just makes the looped part again
-repair either lengthens template strand or cuts stem loop off

single-stranded DNA stem loops before DNA pol comes along, so it doesn't copy the stem loop
-repair cuts off stem loop or lengthens the daughter strand to fit

Front 60

List types of chemical mutagens and physical mutagens

Back 60

base modifiers
base analogues
intercalating agents

X-rays, gamma rays, UV rays (non-ionizing)

Front 61

what does nitrous acid do?

Back 61

modifies bases
C into U
A into H (acts like G)

transition, affects A and C

Front 62

what does 5-bromouracil do?

Back 62

T into 5BU
5BU binds to G as tautomeric shift

Front 63

two enzymes that do direct repair are ______

Back 63

DNA photolyase (for thymine dimers) and alkyltransferase (for effects of alkylating agents)

Front 64

the proteins involved in base excision repair are ____________

Back 64

N-glycosylase (removes abnormal base)
AP endonuclease (cuts just before the ap site)
polymerase (I in prok, β in euk, δ or ε in euk but needs flap endonuclease)
ligase

Front 65

the proteins involved in nucleotide excision repair are __________

Back 65

UvrA and UvrB complex scans
(UvrA leaves and UvrC binds)
UvrC cuts
UvrD is a helicase
DNA polymerase
ligase

Front 66

the proteins involved in mismatch repair are __________

Back 66

MutH binds hemimethylated GATC
MutL is bridge
MutS binds damage
MutH cuts
MutU separates strands at cut
an exonuclease chews up the daughter strand
DNA polymerase and ligase

Front 67

how are actively transcribed genes fixed faster?

Back 67

transcription-repair coupling factor
recruits NER system

Front 68

sloppy DNA polymerases that can copy crappy DNA are called __________

Back 68

translesion DNA polymerases

Front 69

name all the repair systems

Back 69

Direct repair
Base excision repair
Nucleotide excision repair
Mismatch repair
NHEJ
HRR