Midterm 2 Flashcards

1
Q

3 ways regulation of promotor region by DNA modification

A
  1. methylation
  2. DNA inversion
  3. local sequence variation
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2
Q

3 mechanisms for sigma factor release from antisigma factor

A
  1. proteolytic cleavage
  2. chemical interaction
  3. partner swapping
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3
Q

3 sites in ribosome

A

aminocyl site
peptidyl site
exit site

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4
Q

translation control: growth rate-dependent control of 70S ribosome

A

ribosomal proteins can bind to their won mRNA and prevent translation.
Higher levels of ATP promote translation. Lower levels inhibit.

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5
Q

translation consensus sequence

A

AGGAGG- critical for ribosome binding.

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6
Q

two types of M tRNA

A

initiator tRNA, elongator tRNA

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7
Q

translation - 3 elongation steps

A

aminoacyl-tRNA binding
transpeptidation
translocation

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8
Q

trigger factors

A

-ensure proper de novo protein folding
-2-3x more TF than ribosomes in cells
-

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9
Q

DnaK

A

hydrophobic core

sandwich subdomain, helical lid domain which compose the substrate binding domain.

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10
Q

DnaJ

A

cystein rich

zn finger domain

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11
Q

DnaK, DnaJ, GrpE - mechanism

A

DnaK is a holdase
DnaK is bound to ATP. DnaJ brings in protein to be folded. ATP is used to fold protein. DnaJ is released. GrpE facilitates the ADP ATP exchange.

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12
Q

signal sequence

A

N terminal marks the protein for secretion

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13
Q

tat system

A

transports proteins out of the cell - usually with cofactor.
powered by the PMF

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14
Q

how does the N terminus affect protein turnover

A

some AA are unstable (RKFLWY) and have a short half life.

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15
Q

4 reasons for protein degradation

A
  1. misfolded/unfolded
  2. denatured or damage
  3. missing their partner
  4. not needed anymore by the cell (process is complete
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16
Q

AAA protease

A

ATPases Assocated with a number of cellular activites

17
Q

sspB

A

modulate kinetics of substrate binding y the protease

18
Q

RssB

A

absolutely required for substrate recognition and proteolysis

19
Q

regulated proteolysis mechanism

A
  1. truncated protein
  2. tagged with SsrA by tmRNA
  3. SspB binds to substrate to mark for the protease
  4. Proteolysis in protease with RssB and ATP.
20
Q

enzyme regulation

A

activity

amount

21
Q

allosteric effect

A

end product acts as an allosteric effector for the enzyme that is catalyzing the reaction, binding and changing the conformation of the enzyme.

22
Q

covalent modifications of enzymes

A

methylation, AMP/ADP addition, phosphate group addition

23
Q

corepressor

A

a repressor may need a corepressor to bind to it so it cna bind and block transcription.

24
Q

inducer

A

bind to repressor and prevent them binding to DNA, allowing transcription

25
Q

lac operon

A

-needs lactose present and high cAMP-CRP

-

26
Q

arabinose operon

A

AraC is both activator and repressor
can for loop through dimerization
can bind to I and promote transcription of araBADa

27
Q

Embdem-Meyerhof Pathway

A

glucose is used as precursor to form precursors for TCA.
gluconeogenesis - formation of glycogen/starch
can produce pyruvate, lactate, glycerol etc.

28
Q

net yield of glycolysis

A

2ATP
2 pyruvate
2NADH
2 H2O

29
Q

Cra and regulatory pathways

A

when glucose and lactose are present: Cra is off - repression of gluconeogenesis, ED and EM activated
when lactose is present: Cra is off- same as above
when neither is present: Cra is on - gluconeogenesis is activated, ED and EM off.

30
Q

Cra - where does it bind? how do catabolites affect function

A

upstream of RNAP activator, downstream = inhibitor.

-catabolites bind and repress gluconeogenic genes and activate glycolytic genes.

31
Q

CsrA

A

going to activate anything relating to growth - glyocolysis and pathogenesis

32
Q

ED Net

A

1 ATP

1NADH

33
Q

ED genes

A

all genes are not essential

34
Q

ED genes

A

all genes are not essential

35
Q

Pentose phosphate NET

A

ribulose 5-P, CO2, 2NADPH, 1ATP

36
Q

TCA NET (including the pre step)

A
2 pyruvvate
6 CO2
8. NADH
2FADH2
2 GTP
37
Q

FNR

A

Fumarate and nitrate reductase

TCA regulator

38
Q

ArcA

A

aerobic respiration control, member o two component regulatory system responding to oxygen availability.