Final Exam : Exam 5 pt 2 Flashcards

1
Q

Why is it not enough to control regulation of sugars individually

A

because the sugars often have a preferred substrate

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2
Q

Global regulatory mechanisms

A

-complex control system that regulates expression of cellular processes in microorganisms
-one event that triggers all proteins

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3
Q

best sugar

A

glucose

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4
Q

global regulatory mechanisms also called

A

catabolite repression

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5
Q

Catabolite repression

A
  • mechanism that controls sugar usage
    -helps us use glucose above all else
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6
Q

Catabolite repression is an example of

A

-positive of control of transcription
-activator protein

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7
Q

activator protein of catabolite repression

A

Cyclic AMP receptor protein

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8
Q

Cyclic AMP receptor protein

A

-common regulatory nucleotide
-also called cyclic GMP, di-GMP, and guanosine tetraphosphate

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9
Q

effector protein

A

cyclic AMP, tied to glucose

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10
Q

Cyclic AMP when glucose is present:

A

-Low cyclic AMP
-glucose inhibits adenylate cyclase (inhibit cAMP production)
-glucose causes the transport of remaining cAMP out of cell
-no RNA polymerase brought in bc no binding to activator
**seen before Lac operon

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11
Q

Cyclic AMP when glucose is abscent

A

-High cyclic AMP
-cAMP acts as inducer and draws in RNA polymerase

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12
Q

Glucose and lactose present

A

-no lactose utilization enzymes
-only glucose enzymes

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13
Q

No glucose but lactose is present

A

-no inhibition of adenylate cyclase
-lactose utilization genes will be made

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14
Q

if neither lactose or glucose present

A

repressor will be sitting on the operator

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15
Q

diauxic growth

A

-more exponential growth seen with glucose
-lag phase
-then less exponential growth w lactose

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16
Q

lag phase

A

when glucose runs out and have to wait for lactose to be brought in

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17
Q

two compartment regulatory system

A

links events occurring outside the cell to the regulation of gene expression inside the cell

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18
Q

two players in two compartment regulatory systems

A

-sensor kinase proteins
-response regulator proteins

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19
Q

sensor kinase proteins

A

-inside cell membrane (integral protein)
-autophosphorylation upon recognition of environmental cue

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20
Q

kinase

A

-phosphorylate proteins
-typically phosphorylate themselves (autophosphorylation)

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21
Q

categories of kinases

A

-serine-threonine
-tyrosine
-histidine

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22
Q

what residue doe phosphorylation occur at in sensor protein kinases

A

histidine residue

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23
Q

response regulator protein

A

-Cytoplasmic
-DNA binding protein
-effector is passing of phosphorylation

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24
Q

how do you reset system

A

feedback loop and phosphotase

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25
phosphatase
removing phosphate from response regulator at a constant rate
26
mutations
-inherited change in the nucleotide base sequence of the genome -relatively rare bc of proofreading mechanisms -driving force of evolution
27
how often is there a mutation
every 108-109 base pairs
28
what do we have to fix mutations
repair mechanisms
29
why do we see more in prokaryotes than eukaryotes
-no backup copies of genes: haploid -replicate very fast
30
mutant strain
-bacteria carrying mutation strain -genotype will differ, phenotype may not differ
31
point mutations
when one base pair is substituted for another
32
silent mutation
-different sequence but allows for same amino acid to be coded for -occur in wobble site
33
nonsense mutation
mutation allows a stop codon to be placed there causing for a incomplete protein
34
missense
-add in a different amino acid -different amino acid than before
35
frameshift mutations
-when base pairs are inserted or deleted -alters the reading frame
36
reverse mutations
when an earlier mutation is reversed by a second mutations
37
two types of reverse mutations
1. same-site (true) reversion 2. second-site reversion
38
same site reversion
converts the mutant nucleotide sequence back to original sequence
39
second site reversion
a second mutation occur at a different site in the DNA and causes the first mutation to be restored
40
second mutation found in
same gene or another gene
41
spontaneous mutation
-random change in DNA arising from errors in replication -intrinsic -quite slow (10-6 - 10-8)
42
induced mutations
-exposure to mutagens (physically or chemically) that interact with DNA in a disruptive manner
43
base analogs
-compounds that look similar to base used in DNA but have an extra group that attaches that modifies and causes a stable mutation -point mutations -need to be actively growing bc it cant be incorporated into dormant cell
44
DNA modifying agents
-mutagens that change the baes structure and therefor alter its base pairing -addition of a group that attaches to a base that's already there
45
Intercalating agents
-planar molecules that insert themselves between the stacked bases of the helix to induce single nucleotide pair insertions and deletions -frameshift mutation -disrupts DNA polymerase
46
non-ionizing Radiation
-excites an atom to a higher energy state -UV radiation (260nm) -not as penetrating a ionizing -absorbed by DNA and targets pyrimidines bases forming pyrimidine dimers
47
ionizing radiation
-radiation ejects orbital electrons from an atom and causes ions to form -gamma rays (most) -X rays -cathode rays (least)
48
why must we have repair mechanisms
-because mutations can alter nucleotide sequences, they must be able to repair any lethal changes
49
nucelotide excision repair
-UvrABC enzyme detects issue and cleaves out section -fills in with DNA poly I -DNA ligase makes final connection
50
base excision repair
-DNA glycosylase removes just the base yielding an apurinic/apyrimidinic site (AP site)
51
AP endonucleases
-recognizes AP site, and nicks the DNA backbone -DNA poly I put in correct nucleotide -DNA ligase makes final connection
52
Direct repair
photoactivation
53
photoactivation
-light activated repair -photolyase -used for dimers
54
SOS repair system
-seen in extreme conditions and a lot of errors -Rec A protein -Lex A protein -Sfi A -Translesion DNA synthesis genes
55
Rec A protein
-activated due to stalls in replication -triggers Lex A repressor to cleave itself to initiate gene transcription -increases transcription of genes for excision repair -produces Sfi A
56
Lex a repressor
found in operator region of SOS gene
57
Sfi A
blocks cell division
58
Translesion DNA synthesis
breakage and no longer have a template, use DNA poly IV and V which have no proofreading capabilities
59
selection mutant isolation
-confers to an advantage for the organism -antibiotic resistance
60
screening mutant isolation
-examining large numbers of colonies for certain types of mutations -non-selectable -nutrient deficiencies
61
Replica plating
used ti detect auxotrophic mutants
62
A lysine auxotroph only grows on
lysine supplemented media