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BIMM 120 - Microbio > Final Exam Material > Flashcards

Final Exam Material Flashcards

1
Q

Are bacterial circadian clocks functionally the same as ours?

A

YES

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2
Q

circadian clocks/rhythms in cyanobacteria are…

3 Points

A
  1. innate
  2. endogenous
  3. cannot be changed by environment, except for temp
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3
Q

why are circadian clocks important for separating oxygen rxns from nitrogen rxns?

A

photosynthesis for oxygen fixation during the day

Nitrogen fixation during the night given oxygen fixation does not occur

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4
Q

what is the the circadian-infradian rule?

A

Infradian means cycle time greater than 1 day
Thus, it makes no sense for a cell to have a circadian rhythm if its lifetime/reproduction time is shorter than 1 day

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5
Q

KaiA protein structure

A

a dimeric protein

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6
Q

KaiB protein structure

2 total

A

an inactive tetramer
an active monomer

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7
Q

KaiC protein structure

3 total

A

a hexamer

has an internal duplication leading to double-donut shape

has ATP binding motifs - core oscillator

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8
Q

which ends of KaiC are the CI/CII ring? where is the A- and B-loops?

A

Bottom donut = CI ring
–> B-loop
Top donut = CII ring
–> A-loop = C-terminus of CII ring

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9
Q

what binds to the A- and B-loops?

A

KaiB binds to phosphorylated KaiC @ the B-loops when exposed, adding another stacked toroid to KaiC

KaiA binds to A-loops when exposed, restarting the cycle

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10
Q

what aa are phosphorylated and in what order?

A
  1. Thr-432 (Threonine)
  2. Ser-431 (Serine)
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11
Q

SasA - what is it? what is its function? what is the effect on the diff classes of genes?

dont forget what happens w/ increasing phosporylation of CII

A

histidine kinase

phosphorylate TF - RpaA - that binds upstream of genes

@ day, binds to CI of KaiC and autophosphorylates, transfering its phosphate group to RpaA

more CII phosphorylation, more SasA phosphorylates RpaA

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12
Q

CikA - what is it? what is its function? what is the effect on the diff classes of genes?

A

histidine kinase + phosphatase
acts on RpaA - that binds upstream of genes

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13
Q

RpaA - what is it? what is its function? what is the effect on the diff classes of genes?

A

a responsive regulator

governs transcription from a locus that controls global changes in circadian rhythm gene expression

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14
Q

KaiABC system - @ dawn

A

Dawn: KaiC is UNphosphorylated w/ loosely connected CI/CII rings. KiaA binds exposed A-Loops

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15
Q

KaiABC system - @ morning

A

Morning: KaiA binding stimulates KaiC autokinase activity, phosphorylating Thr-432 1st

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16
Q

KaiABC system - @ daytime

A

Daytime: Phosphorylation changes KaiC structure, facilitating phosphorylation of Ser-431.

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17
Q

KaiABC system - @ dusk

A

Dusk: both residues are phosphorylated. Increased CII ring stiffness leads to stacking of CII on CI, tucking A-Loops in, hiding the KaiA binding site. B-Loop on C1 is exposed.

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18
Q

KaiABC system - @ night

what dissociates? what type of activity starts?

A

Night: KaiA dissociates due to A-Loop inaccessibility. KaiB binds the exposed B-Loop. KaiC autokinase activity ceases, and autophosphatase activity begins. Thr-432 gets dephosphorylated 1st

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19
Q

KaiABC system - @ late night

A

Late Night: Ser-431 gets dephosphorylated - The cycle restarts

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20
Q

Are TTFLs delayed-negative feedback loops?

A

YES

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21
Q

Does KaiABC act as a self-sustained PTO?

A

YES

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22
Q

Where does Ser/Thr autophosphorylation and autoDEphosphorylation occur?

A

occurs @ CII

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23
Q

about how long this whole cycle takes?

A

24 hrs to complete

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24
Q

when is CII maximally and minimally phosphorylated?

A

CII max phosphorylated @ dusk
CII min phosphorylated @ dawn

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25
Q

KaiB changes form between…

A

a tetramer + a monomer

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26
Q

what are the 3 intertwined functions of any circadian clock?

A

timekeeping, entrainment, and output signaling

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27
Q

Can KaiB monomers outcompete the SasA bound to the B-loop of CI?

A

YES

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28
Q

What are 2 ways in which clock entrainment can be completed?

A
  1. Through sensitivity of the phosphorylation cycle to ATP/ADP ratios - Alignment max photosynthesis w/ highest ratio
  2. Through the presence of nighttime-associated photosynthetic metabolites
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29
Q

ICMs - what are they?

A

intracellular membranes

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30
Q

what happens when there is an accumulation of proteins?

A

Overproduction of protein can result in the formation of inclusion bodies

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31
Q

what are chromatophores? what are they responsible for?

via what process?

A

a type of ICM - a intracellular photosynthetic apparatus

responsible for generating skin + eye color via catalyzing light-driven rxns including PMF-driven ATP synthesis

32
Q

do chromatophores have a diff lipid + protein composition compared to cytoplasmic membranes? how so?

A

YES

Some continuous, others discontinuous w/ plasma mem

33
Q

what are magnetosomes? what are the crystals surrounded by? what does that suggest?

A

allow organisms to align w/ Earth’s magnetic field

magnetite/greigite crystals are surrounded by a mem of lipids (similar to those of the plasma membrane) but contain unique proteins

suggests they likely arose from plasma membrane invagination

34
Q

magnetosomes: what direction do they orient to in the northern hemisphere? what direction do they swim towards? why is direction important?

A

NH - orient northward and swim towards the south pole of a magnet

Important to search for nutrient-rich sediments

35
Q

what are anammoxisomes?

A

anammoxosomes - energy-producing mitochondrion-like organelles (given their lipids)

ladderanes - unusually rigid lipids bc of their inflexible ladder-like structure that contribute to energy conservation via creating a more H+ leak-proof membrane

36
Q

what process do anammoxisomes use to establish a PMF used to make ATP?

A

quinone-dependent process

37
Q

why do Anammoxosomes compartmentalize enzymes?

A

for catalysis of NH4+ (ammonium) oxidation, allowing for energy production to aid in anaerobic NH4+ oxidation

38
Q

do all membranous organelles (chromatophores, magnetosomes, anammoxisomes) have unique lipid and protein compositions?

A

YES

39
Q

What are ALL the ways in which bacterial OMVs can be utilized? 5 total

A
  1. Delivery of toxins to eukaryotic cells
  2. Protein + DNA transfer between bacterial cells
  3. Trafficking of cell-cell signals
  4. Delivery of proteases and antibiotics
  5. Removal of harmful incorrectly folded proteins
40
Q

what are acidocalcisomes? what is their function? what do they resemble?

A

calcium/polyphosphate rich acidic membrane-enclosed organelles (in all domains of life)

function –> to store cations + polyphosphates

resemble lysosomes in their size + acidic properties + contents

41
Q

what are mesosomes? how did they arise in (+) bacteria?

A

intracellular extensions of the plasma membrane in (+)/(-) bacteria

gram-(+) bacteria resulted from invagination of the plasma membrane

42
Q

what happens to magnetosomes during cell division?

A

the chain breaks into 2, each going to 1 daughter cell

43
Q

virulence factors of bacteria + function?

5 total points

A
  1. Adhesins - recognize glycolipids and glycoproteins on the surface of cells they infect
  2. Invasins - adhesins that allow entry into cells
  3. Cytotoxins - specific inhibitors of cellular processes
  4. Proteases - modify the cell surface and destroy host cell defense functions
  5. Suppression of host defense mechanisms to promote pathogen survival
44
Q

what are the 3 types of adhesins?

A
  1. Outer envelope proteins
  2. Rigid rod-like fimbriae (pili)
  3. Flexible helical fimbriae
45
Q

what is the asymmetric division of Caulobacter crescentus?

A

always produces 1 motile swarm cell + a sessile stalked cell

46
Q

what kinds of compounds are used in quorum sensing?

A

small, diffusible organic molecules called autoinducers

47
Q

what is the difference between bet-hedging and division of labor?

A

bet-hedging: adopting phenotypic heterogeneity to deal w/ environmental fluctuations

division of labor: concurrently interact with each other by exerting different functions

48
Q

what is an examples of bet-hedging? division of labor?

A

BH: expression of different metabolic capacities in E. coli ex 2. presistnace

DOL: energetically costly production of the T3SS of S. typhimurium

49
Q

what is the relationship between quorum sensing and phenotypic heterogeneity?

A

Quorum sensing (usually a coordinator of bacterial collective behavior) can be a driver or target of phenotypic heterogeneity

50
Q

is quorum sensing a positive feedback mechanism?

A

YES

51
Q

what is public goods? private goods? cheaters? in terms of quorum sensing

A

PubG - primarily regulates shared features via production of energetically costly “public goods”

PriG - regulate energetically costly “private goods” which are not shared, but the pop as a whole can still benefit

Cheaters - invading members that don’t contribute to costly production of public goods but still benefit from
them, thus, a fitness advantage

52
Q

can phenotypic heterogeneity also be caused by stochastic switching of gene expression?

A

YES

53
Q

What are the basics of persisters? include transition between state characteristics.

WHAT IS THE TRANSITION BETWEEN STATES???????????

A

comprise individuals in a clonal, antibiotic-tolerant bacterial population that survive exposure to [high bactericidal antibiotics]

Persister tolerance is temporary + Dormant/slow growing

randomly determined and does not involve a genetic change + all bacteria could still have persistence

54
Q

what does bacteria influence? how?

A

their environment by autoinducers

55
Q

following bacteria influencing their environment, autoinducers then influence…

A

the cells

56
Q

the progression of the asymmetric cell division of Caulobacter crescentus is controlled…….and needs to be……..

A

sequentially; localized to a pole

57
Q

what happens if the cell division is blocked early or late?

A

If blocked early, flagella and pili canNOT be assembled

If blocked later, they still can be assembled

58
Q

what is division scar?

A

division scar - organization centers formed during cell division that serve as markers for new cell poles

59
Q

what are the characteristics of TipN and TipF?

A

TipN - marker protein for spatial and temporal differentiation

TipF - a c-diGMP phosphodiesterase that regulates cell cycle

60
Q

what are the additional functions of TipN and TipF?

aka for tipN, what happens if its lacking? what can’t negative TipF mutants make? what anchors TipN + TipF? what happens apon anchoring?

A

TipN - w/o TipN, polarity is lost and inversion sites for the new membrane is randomized

TipF negative mutants cannot make flagella

new septum anchors TipN, which anchors TipF

anchoring lowers [c-diGMP] so the flagellum can be made

61
Q

What does TipN localization depend on (2 things)? what does it determine + localize (3 things)? what happens if it is over expressed?

A

TipN localization depends on FtsZ + FtsI

TipN also determines the asymmetric cell division site + localizes some regulatory proteins and actin-like proteins like MreB

If TipN is overexpressed, there are many new poles w/ cell branching and each pole can then assemble a flagellum

62
Q

What does FtsZ form? what is Ftsl?

A

FtsZ - septum
Ftsl - septum cell wall synthesis protein

63
Q

what are the rules of Anabaena cell division? 3 total

in terms of whether you will have a large or small daughter cell

A
  1. If a cell arises as the left (L) daughter cell its left daughter cell will be small
  2. If a cell arises as the right (R) daughter cell, its right daughter will be small
  3. Heterocysts always develop from a small cell. Therefore, the two daughter cells have different developmental potential
64
Q

what are MinC/MinD/MinE? what is the purpose of the mechanism?

A

purpose: a mechanism that prevents separation (cell division) from occurring at the poles

E - a topological specificity determinant
D - an ATPase that interacts with C and E, and stimulates MinC/D release from the membrane
C - a FtsZ polymerization inhibitor

65
Q

how does Caulobacter crescentus produce either a swarmer cell or a stalked cell?

A

via asymmetic cell division

66
Q

how do CheA and CheW participate in protein localization?

A

A conserved domain near the C-termini of the MCPs - required for polar localization - recognizes CheW + CheA

67
Q

what is the regulation of proteolysis in Caulobacter crescentus?

A

proteolysis is both temporally (in the swarmer cell) and spatially (in the stalked cell) regulated

68
Q

PleC/D? SK/RR pairs

what does it direct? what does it control? what does it initiate?

A

directs pilus, flagellum and MCP synthesis and controls proteolysis - initiates swarm cell biosynthesis

69
Q

DivJ/K? SK/RR pairs

A

is essential for cell cycle progression

70
Q

CckA/CrtA? SK/RR pairs

A

controls gene expression + silences oriC in the swarmer cell

71
Q

what are the biofilm/planktonic state transition?

A

w/ c-diGMP - biofilm
w/o c-diGMP - planktonic state

72
Q

what are the factors that persistence in E. coli depend on?

4 total

A

(1) the nucleotide 2 nd messenger (p)ppGpp
(2) Lon protease
(3) polyphosphate (P)
(4) toxin/antitoxin pairs

73
Q

what are all of the enzymes used (2 total) in ppGpp homeostasis? what are the first 4 steps?

A

Enzymes: RelA + SpoT

  1. ppGpp activates T/AT (toxin/antitoxin) loci involving polyP + Lon
  2. ppGpp inhibits exopolyphosphatase (PPX)
  3. More PolyP made by polyP kinase (PPK)
  4. PolyP binds w/ Lon, increasing Lon protease activity
74
Q

what are the basics about significant plagues in history?

what kind of diseases were they?

4 plagues total

A

***were all likely infectious diseases

430 BCE - The plague of Athens where immunity was observed

Bubonic = rat-flea-man

Pneumonic = man to man, coughing
The Great Plague of Londone

The Black Death (Bubonic Plague in Europe) w/ Buboes = lymph nodes + Hemorrhagic necrosis of the extremities

75
Q

What are the last 4 steps (5 - 8 steps) of ppGpp homeostasis

A
  1. Lon protease degrades eleven ATs of E. coli K12
  2. More toxins (site specific RNases) are present
  3. mRNA cleavage inhibits translation, which slows/stops cell growth
  4. If ppGpp is low, cells revive and grow
76
Q

what are the “thinking like bacteria” points? 2 points

A

Do not disfigure your host too much bc then people would know you are infected + you cannot spread the disease as much

Also can use toxins to force you to cough, which then helps with the spread

77
Q

what are Koch’s Postulates used to determine if a disease is caused by a specific microbe (3 total) and his corollary?

A

postulates:
1. isolate the organism from the diseased tissues
2. Grow the organism outside the host
3. Inoculate the organism into a new, healthy host
4. Reproduce the disease in the new host

Corollary: you should be able to make a vaccine and prevent the disease

BIMM 120 - Microbio (6 decks)

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