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Microbiology > Final Exam : Exam 5 pt 2 > Flashcards

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
Q

phosphatase

A

removing phosphate from response regulator at a constant rate

26
Q

mutations

A

-inherited change in the nucleotide base sequence of the genome
-relatively rare bc of proofreading mechanisms
-driving force of evolution

27
Q

how often is there a mutation

A

every 108-109 base pairs

28
Q

what do we have to fix mutations

A

repair mechanisms

29
Q

why do we see more in prokaryotes than eukaryotes

A

-no backup copies of genes: haploid
-replicate very fast

30
Q

mutant strain

A

-bacteria carrying mutation strain
-genotype will differ, phenotype may not differ

31
Q

point mutations

A

when one base pair is substituted for another

32
Q

silent mutation

A

-different sequence but allows for same amino acid to be coded for
-occur in wobble site

33
Q

nonsense mutation

A

mutation allows a stop codon to be placed there causing for a incomplete protein

34
Q

missense

A

-add in a different amino acid
-different amino acid than before

35
Q

frameshift mutations

A

-when base pairs are inserted or deleted
-alters the reading frame

36
Q

reverse mutations

A

when an earlier mutation is reversed by a second mutations

37
Q

two types of reverse mutations

A
  1. same-site (true) reversion
  2. second-site reversion
38
Q

same site reversion

A

converts the mutant nucleotide sequence back to original sequence

39
Q

second site reversion

A

a second mutation occur at a different site in the DNA and causes the first mutation to be restored

40
Q

second mutation found in

A

same gene or another gene

41
Q

spontaneous mutation

A

-random change in DNA arising from errors in replication
-intrinsic
-quite slow (10-6 - 10-8)

42
Q

induced mutations

A

-exposure to mutagens (physically or chemically) that interact with DNA in a disruptive manner

43
Q

base analogs

A

-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
Q

DNA modifying agents

A

-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
Q

Intercalating agents

A

-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
Q

non-ionizing Radiation

A

-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
Q

ionizing radiation

A

-radiation ejects orbital electrons from an atom and causes ions to form
-gamma rays (most)
-X rays
-cathode rays (least)

48
Q

why must we have repair mechanisms

A

-because mutations can alter nucleotide sequences, they must be able to repair any lethal changes

49
Q

nucelotide excision repair

A

-UvrABC enzyme detects issue and cleaves out section
-fills in with DNA poly I
-DNA ligase makes final connection

50
Q

base excision repair

A

-DNA glycosylase removes just the base yielding an apurinic/apyrimidinic site (AP site)

51
Q

AP endonucleases

A

-recognizes AP site, and nicks the DNA backbone
-DNA poly I put in correct nucleotide
-DNA ligase makes final connection

52
Q

Direct repair

A

photoactivation

53
Q

photoactivation

A

-light activated repair
-photolyase
-used for dimers

54
Q

SOS repair system

A

-seen in extreme conditions and a lot of errors
-Rec A protein
-Lex A protein
-Sfi A
-Translesion DNA synthesis genes

55
Q

Rec A protein

A

-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
Q

Lex a repressor

A

found in operator region of SOS gene

57
Q

Sfi A

A

blocks cell division

58
Q

Translesion DNA synthesis

A

breakage and no longer have a template, use DNA poly IV and V which have no proofreading capabilities

59
Q

selection mutant isolation

A

-confers to an advantage for the organism
-antibiotic resistance

60
Q

screening mutant isolation

A

-examining large numbers of colonies for certain types of mutations
-non-selectable
-nutrient deficiencies

61
Q

Replica plating

A

used ti detect auxotrophic mutants

62
Q

A lysine auxotroph only grows on

A

lysine supplemented media

Microbiology (20 decks)

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