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ZZPathology undergraduate year 3, first term. > Bacteriology - signalling, motility, half of adhesion. > Flashcards

Bacteriology - signalling, motility, half of adhesion. Flashcards

1
Q

TFs bound by small molecules

A

LacI, a repressor

Fur

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2
Q

LacI signalling pathway

A

Allolactose binding LacI repressor prevents DNA binding and hence prevents repression. proteins involved in lactose metabolism.

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3
Q

Fur signalling pathway

A

In the host there is little iron. Iron binding (outside host) increases Fur binding to DNA. This represses virulence gene expression. One of these genes is pvdS.

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4
Q

PvdS role

A

a sigma factor in Pseudomonas aeruginosa increasing transcription of toxR, prpL endoprotease (for tissue destruction) and genes for pyoverdine biosynthesis.

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5
Q

Examples of second messengers

A

cAMP, c-di-GMP, c-GMP, c-di-AMP.

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6
Q

cAMP synthesis and breakdown

A

Synthesised from ATP by cya in response to carbon limitation.
Broken down by CpdA to AMP.

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7
Q

cAMP signalling pathway

A

cAMP binds CRP (cAMP response protein) which binds promoters.
Results: activates catabolism from other sources, flagellar and virulence genes. Represses biofilm formation.

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8
Q

c-di-GMP synthesis and breakdown

A

Synthesised by diguanylate cyclases, with a sensing domain and a GGDEF domain for catalysis. Synthesis is via a 5’ pppGpG intermediate.
Phosphodiesterases with EAL or HD-GYP motifs breakdown.

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9
Q

c-di-GMP effects

A

Oppose cAMP: shift to less virulence. Also binds effector proteins.

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10
Q

Example of TF affected by c-di-GMP

A

VpsT is bound and stabilised as a dimer for transcription of the vps operon. Vps binds biofilm together in cholera.

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11
Q

Example of cellular protein affected by c-di-GMP signalling

A

c-di-GMP bound by EAL domain of FimX, which binds PilZ which interacts with PilB to stimulate pilus growth.
YcgR has PilZ domain. Acts as brake on flagellar motor when c-di-GMP is present.

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12
Q

RNA riboswitches

A

3D RNA structures that affect translation. May form in such a way that terminator or Shine-Delgardo sequences cannot be read.

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13
Q

Example of RNA riboswitch signalling.

A

c-di-GMP binds GEMM motif very tightly, regulating translation of flagella and pilus genes.

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14
Q

HK in HAP pathways

A

ATP binding domain, sensory input domain, phosphotransfer domain.

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15
Q

RR in HAP pathways

A

Response regulators. Have receiver domain and output domain.

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16
Q

HAP pathways in virulence

A

TrxSR two component system
EnvZ-OmpR –> SsrA/B –> SPI-2.
Cholera CAI-1 (Cqs) and AI-2 (LuxS)

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17
Q

DNA dep RNA pol initiation of transcription

A

Formed of ββ’α2ω. . Interaction with σ factor leads to formation of holoenzyme. σ factor recognizes specific promoter sequences, positions RNAP on DNA and facilitate unwinding near the start site. RNA pol recognizes -10, -35 and also extended -10 (recognized by σ) and UP element (recognized by α subunit).

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18
Q

RNAP and sigma factors are in short supply. What determines transcription?

A

Promoters, which sigma factors are present, small ligands, transcription factors and chromosome structure.

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19
Q

Control of sigma factors

A

By transcription. By anti-sigma factors.

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20
Q

Role of small ligands in controlling transcription

A

Very general. Some alter stability of RNAP complexes. E.g. ppGpp destabilises the open complex so globally decreases transcription. Starvation response.

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21
Q

Example of co-operation between signalling pathways

A

cAMP and LacI. If lactose is present LacI is sequestered, but when it is not, and cAMP binds CRP, cAMP-CRP bends the DNA so that the RNAP binds it better.

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22
Q

Example of phosphorylation of other pathways

A

Stks phosphorylate response regulators in HAP pathways.

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23
Q

Complications to signalling

A

Pathways: longer, intermediary steps. Co-operation with other pathways. Amplification. Positive feedback.
Complication to signals: response to QS depends on bacterial strain. Autoinhibitors, cholera.

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24
Q

Biosynthetic gene clusters

A

Microbiome constantly signalling within itself and to the host: recent study showed there are many biosynthetic gene clusters. We do not understand them all.

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25
Q

Quorum sensing

A

Method of taking bacterial census to enable multicellular behaviour.

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26
Q

Quorum sensing: bacterial-host interaction.

A

Vibrio fischeri colonise light organ of squid for hunting trips. Uses Lux system.

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27
Q

The 4 canonical QS systems

A

AIs which diffuse out, AIs which act on HAP systems, AIPs, reimported AIPs.

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28
Q

AIs which diffuse - general structure.

A

AI synthase make AHL: diffuses out, diffuses in, acts on receptor.

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29
Q

Examples of AIs which diffuse.

A

LuxI-LuxR, LasI-LasR, RhlI-RhlR

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30
Q

Details of Lux system

A

Lux I is auto-inducer synthase makes AHL by catalysing formation of amid bond between SAM and acyl-ACP. AHL diffuses away.
LuxR is a receptor – promotes lux operon expression. Has ligand binding domain and DNA binding domain that interacts with RNAP
LuxI homologues in different bacteria make different AHL homologues.

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31
Q

AIs which act on HAP systems - general outlines

A

 AI synthase makes AI, it diffuses out but acts on HKs, which act on response regulators.

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32
Q

Examples of AIs which act on HAP systems

A

CAI-1 system in V. cholerae.

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33
Q

Details of CAI-1 system in V cholerae.

A

 CqsA makes CAI-1 which diffuses out. Binds and represses CqsS, an HK, which phosphorylates LuxU, which activates LuxO-P which activates Qrr1-4, whiach activates AphA (a TF), activating TcpP/H (a TF) and increasing ToxT (a TF) synthesis.

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34
Q

AIPs - general outline.

A

Pro-AIP exported, made into AIP, acts on HK.

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35
Q

AIPs - example

A

 Agr system. AgrD exported by AgrB which makes it AIP at the same time. Binds AgrC which phosphorylates AgrA which binds SarA, altering transcription.

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36
Q

AIPs with reimportation. General outline.

A

Pro-AIP secreted, altered outside cell, reimported, acts on receptor.

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37
Q

AIPs with reimportation. Examples.

A

. in Bacillus cereus PapR is secreted, is converted by NprB inot AIP, reimported by Opp, and allowed to work on TFs to alter gene expression. TFs like PlcR.

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38
Q

PQS quinolone system

A

PqsABCDH makes PQS which diffuses out. PQS binds PqsR. An AI which isn’t an AHL.

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39
Q

Control of alpha toxin production in Staph aureus.

A

AgrA binds SarA, increases transcription of Agr operon and RNAIII. RNAII binds part of alpha hemolysin mRNA stem loop, resulting in a conformational switch that makes the Shine-Dalgarno sequence available for translation.

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40
Q

Examples of QS increasing virulence.

A

Virulence gene expression by complex P aeruginosa system.

PlcR AIP in Bacillus cereus

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41
Q

LuxS system in V cholerae

A

LuxS makes AI-2 which binds and inhibits LuxPQ. LuxPQ usually activates Lux U (convergence with CAI-1 system), which activatees LuxO-P, which activates Qrr1-4, activating AphA (TF), TcpP/H (TF) and ToxT (TF).

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42
Q

AphA

A

Reciprocal inhibition with HapR .

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43
Q

QS decreasing virulence

A

AI-2 and CAI-1 in V cholerae, aids colonisation and biofilm formation.

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44
Q

QS in interspecies communication

A

Detection, kin selection, pathogen-host interaction.

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45
Q

P aeruginosa QS system

A

LasR causes expression of all systems.
RhlR causes expression of itself and inhibition of the PQS system.
PqsR causes expression of itself and of RhlR.

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46
Q

Bacterial kin selection

A

Staph aureus – different serovars produce different AIPs activate signalling in cognate receptors, block signalling in non-cognate receptors.
Potential for universal inhibitor? Lyon et al 2000.

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47
Q

Using QS against bacteria - proof of principle

A

Delisea pulchra produces a halogenated furanon that binds the LR family of TFs and inhibits their function.

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48
Q

QS signals and host cells

A

OdDHL, cyclic dipeptides, QseC.

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49
Q

OdDHL

A

OdDHL by Pseudomonas aeruginosa alters expression of 4500 genes, including those for immunomodulation, inflammation and apoptosis.

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50
Q

Cyclic dipeptides

A

Cyclic dipeptides are produced by all kingdoms of life. Phe-pro is involved in virulence factor signalling in Vibrio cholerae. Cyclic dipeptides in the brain are used to switch to a protective rather than inflammatory response. Could gut microflora affect the CNS? E.g in neurodegenerative diseases.

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51
Q

QseC

A

EHEC QseC HAP sensor kinase responds to both AI-3 and Adr/NA. This leads to increased expression of flagella, toxin and needle genes. Potential: targetting host adrenergic system to manipulate progression of disease.

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52
Q

AgrA activity

A

AgrA binds at upstream of P2 to induce agr operon (Novick et al, 1995)and also activates P3 which controls RNAIII (Novick et al 1993)

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53
Q

CAI-1 in drug development

A

Simplicity and inherent stability mean hopeful for drug development.

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54
Q

Cholera AIs in intervention and control

A

Some evidence that AIs (as yet not identified specifically) can resuscitate dormant Vibrio cholera in water, which could be used in development of intervention and control.

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55
Q

Development of inhibitors of Pseudomonas QS systems.

A

Most are targeted to Las system (although some P. aeruginosa are defective here) either by designing comp inhib. of 3-O-C12-HSL or finding natural inhibitors and modifying them.

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56
Q

Problem with targeting Pseudomonas QS system.

A

Formation of biofilm can be a problem for implants or those with chronic disease. Perhaps only will be of use as co-therapy with something to scatter biofilms e.g. c-di-GMP inhibitors.

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57
Q

P2 and P3 promoters in Staph aureus.

A

Regulation at P2 and P3 promoters by many other transcription factors and sigma factors. Allows response to extracellular signals as well. E.g. extracellular stress leads to expression of σB which has downstream effect of inhibiting expression of toxins (probably affects unknown regulator of agr)..

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58
Q

Targetting AIPs

A

Universal inhibitors. Competitive inhibitors. mAbs against AIPs.

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59
Q

Topics to cover for essays on bacterial flagella-mediated motility and chemotaxis.

A

Types of bacterial motility
Physical requirements
The flagella - structure, mechansim, function.
Controlling motility.

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60
Q

Types of bacterial motility

A

Swimming, swarming, twitching, walking.

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61
Q

Bacteria requiring flagella for transmission

A

Vibrio bacteria - demonstrated in Vibrio anguillarum.

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62
Q

Bacteria requiring flagella for colonisation.

A

To reach epithelium: campylobacter jejuni, H. pylori.

To ascend urinary tract: Proteus mirabilis, UPEC.

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63
Q

Swarming basics

A

Temperate vs robust swarmers.
Requires multiple peritrichous bacteria, cell to cell contact and a slime capsule/biosurfactant.
May involve differentiation.

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64
Q

Swarming differentiation

A

Proteus mirabilis (robust swarmer). Differentiation from vegetative to elongated polyploidy hyperflagellated swarme cells on cell-to-cell contact. Isolation reverses this.

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65
Q

Robust swarmers

A

Cyclical swarming, over biotic or abiotic surfaces, may differentiate.

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66
Q

Temperate swarmers

A

Move continuously in favourable conditions, do not show cyclical swarming.

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67
Q

Twitching basics

A

Uses Type IV pili. Social activity, using rafts of 10-50 cells in twitching zone. Can reach 1 mm/h.

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68
Q

Bacteria which twitch.

A

Pseudomonas aeruginosa. Legionella pneumophila, Neisseria meningitidis, Neisseria gonorrhoea.

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69
Q

Physical requirements for swimming.

A

Fluid to swim in.

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70
Q

Physical requirements for swarming.

A

Water to swim in, decrease in frictional resistance, wetting of uncolonised territory.

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71
Q

Physical requirements for swarming - water to swim in.

A

Sensitive to moistness, hydration via osmotic agents.

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72
Q

Physical requirements for swarming - decrease of frictional resistance.

A

lubrication with surfactants, or increased force with more flagella or special stators.

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73
Q

Physical requirements for swarming - wetting uncolonised areas.

A

Surfactant or substrate with inherently low surface tension is needed to allow this.

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74
Q

Things to remember when writing about flagella.

A

Structure - macro and micro.
Assembly.
Control of assembly.
Function and chemotaxis.

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75
Q

Flagellar patterns

A
  • Monotrichous
  • Lophotrichous
  • Bipolar
  • Peritrichous
  • Periplasmic
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76
Q

Monotrichous flagella

A

V. cholerae

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77
Q

Lophotrichous flagella

A

Pseudomonas

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78
Q

Bipolar flagella

A

Campylobacter

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79
Q

Peritrichous flagella

A

Salmonella and E. Coli

80
Q

Periplasmic flagella examples

A

B. burgdoreferi -7-11 flagella overlapping mid cell.

Treponema pallidum has 3 flagella attached to each pole.

81
Q

Periplasmic flagella

A

Flagella is inbetween OM and peptidoglycan layer. No flagella results in rod-shaped bacteria. Uses serpentine boring motion.

82
Q

Components of flagella basal body

A

L-ring, P-ring, rod, MS-ring, C ring, motor proteins.

83
Q

L-ring

A

Part of basal body. L = lipopolysaccharide. FlgH.

84
Q

P-ring

A

Part of basal body. P = peptidoglycan. FlgI.

85
Q

Rod

A

Part of basal body. Acts as drive shaft, promotes opening of MS ring. FlgC, flgF, flgG, FliE/FlgB.

86
Q

MS ring

A

Part of basal body. Acts as bushing. FliF.

87
Q

C ring

A

FliG, FliM (2 populations), FliN.

88
Q

Motor protein exchange.

A

Not static part of basal body: Δmot speed of rotation increased in discreet jumps with expression of Mot proteins on plasmids.
Dwell time = 30 secs. FRAP experiments showed diffusion in and out.

89
Q

Motor protein action.

A

Harness PMF or Na+ gradient (marine species e.g Vibrio).

Could act via turbine, turnstile or conformation change.

90
Q

Motor proteins.

A

MotB, MotA.

91
Q

Numbers of motor proteins.

A

Varying. Treponema has 16, salmonella 11.

92
Q

C ring - changing direction.

A

Effect of CheY-P binding on FliN is that a conformational change spreads rapidly through the ring, and is passed onto the rotor FliG.

93
Q

ATPase complex in export

A

FliI powers subunit unfolding. Similar to F1.
FliH is a negative regulator of ATPase activity.
FliJ is a positive regulator of ATPase activity.

94
Q

FliH

A

Negative regulator of ATPase activity. Connects ATPase to the C-ring.

95
Q

Hook proteins.

A

FlgE flexible universal joint.

Hook associated proteins linking hook and filament. FlgL, FlgK.

96
Q

Filament proteins (flagella)

A

FliC: bistable with short R form and long L form. R2:L9 is a loos helix, R3:L8 is tighter.
Made of 11 proto-filaments, although assembled as a single helix.

97
Q

Filament cap

A

FliD.

98
Q

Clutch proteins in flagella motor

A

Cause disengagement of stators from motors. EpsE binding FliG causes this, although controversy as to clutch vs brake function.

99
Q

Brake proteins in flagella motor

A

YcgR. C-di-GMP effector, faster than transcriptional changes. Antagonised, probably by H-NS.

100
Q

Flagella assembly cytosolic chaperones.

A

FlgN, FliT and FliS.

101
Q

Secretion system for flagella

A

T3SS.

102
Q

Order of assembly

A

IM ring, cytoplasmic components, rod (distal to proximal), OM rings, hook, HAPs, filament cap, filament.

103
Q

Flagella caps

A

Rod cap degrades peptidoglycan to get through cell wall.
Hook cap is displaced by HAP proteins.
Filament cap stays in place

104
Q

Assembly of flagella direction.

A

Assembly from proximal end.

105
Q

Order of assemby of flagellum.

A

Binding affinities for FlhAc.
Transcriptional hierarchy.
FliK determining switch from hook to filament.

106
Q

Master regulator of flagella transcription.

A

FlhD4C2. Binds DNA motifs upstream of class II and III genes, bending the DNA to recruite RNAP.

107
Q

Switch from class II to class III transcription in flagella synthesis.

A

Class III regulated by sigma factor FliH. Normally sequestered by FliM, but this is exported after hook completion.

108
Q

Class III genes in flagellum.

A

filament, chaperones, motor and chemotaxis.

109
Q

Export pathway of class III genes in flagella synthesis.

A

Chaperones capture subunits, pilot to export machinery, and dock by binding the hydrophobic dimple on FlhAc.
Probable transition of complex from C ring to active ATPase hexamer.
Release of subunit and export, and recycling of chaperone.

110
Q

Powering flagellum synthesis

A

ATPase provides some energy, possibly PMF has a role too: contributions of electrical potential difference and proton gradient are separate.
Refolding of subunits under cap energises pulling uother subunits up channel via head to tail linkage. Must be powered, as independent of flagellum length.

111
Q

FliK

A

Rod-hook secretion substrate.

Communicates hook length completion to flhB, catalysing secretion specificity switch by cleavage of flhB.

112
Q

Models of FliK action.

A

Cup model and molecular ruler model.

113
Q

Model of FliK action - cup model.

A

FliK provides binding sites for FlgE subunits – when sufficient number are bound, the cup was emptied to make hook – but C ring too small to make a cup large enough. Also, can be made without any C ring at all.

114
Q

Model of FliK action - molecular ruler model.

A

Similar to type III injectisome system. Molecular ruler continuously secreted, and interacts with cap. When hook long enough, domain controlling substrate switch comes into contact with flhB.

115
Q

Recruitment of motor proteins

A

Requires presence of driving ion for this, and for retention. Some species automatically switch this on dependent on the environment.
FliM may have 2 populations, static and dynamic.

116
Q

Controlling motility

A

Triggering motility, chemotaxis, other controls

117
Q

Controlling motility - triggering.

A

Different in different states e.g. supermotility in recently excreted planktonic V cholerae. Generally dependent on surface contact, QS and physiological signalling.

118
Q

Chemotaxis - random walk.

A

1-3 s swimming is interspersed with tumbles (0.1s) which randomly reorientate.

119
Q

Chemotaxis - biased random walk.

A

Tumbling less frequent when moving towards attractant, more frequent if moving away. Brownian motion means that will drift off course though, so some tumbling occurs even in strong gradients.

120
Q

MacNabe and Koshland

A

o Bacteria have a temporal memory of 1-4 seconds. Macnab and Koshland experiment in stopped flow chamber in which conc changed so rapidly that there was no spatial gradient.

121
Q

Chemotaxis phosphorelay

A

 Chemotactic signals detected by methyl-acceptiong chemotaxis protein (MCP). CheA is linked to this by CheW. 2 RRs; CheY (immediate continuation of phosphorelay) and CheB (methylesterase – slower comparison system). CheZ allows rapid signal termination.

122
Q

Chemotaxis localisation

A

• Clustering. Implications? Depends on CheW and CheA as well as MCP. Work as trimers (or dimers?) Allow high signal sensitivity and gain of receptors? Integration in receptors.

123
Q

Other controls to chemotaxis.

A

Metabolic state: CheY-p undergoes acetylation. Fumarate binds FRD which binds FliG increasing CW rotation.
CheY can act as brake. Also YcgR.
EpsE acts as clutch.

124
Q

Role of RNA III

A

Activates alpha toxin, represses rot (represses virulence factors). Control of type of virulence; RNAIII activation leads to preponderance of secreted rather than surface virulence factors.

125
Q

How does flagellar rotation switch direction.

A

Binding of CheY-Pi leads to conformations change in FliN

126
Q

Flagellar basal body structures.

A

Outer rings; L-ring and P-ring.
Inner ring; MS-ring
C-ring.
Rod.

127
Q

Chemoattraction in E. Coli

A

MCP receptors and one MCP-like receptor lead to phosphorylation and methylation pathways controlling direction of spin of flagella.

128
Q

Flagella in E. Coli

A

peritrichous rotary nanomotors; spinning CCW –> bundle, spinning CW –> tumble.

129
Q

Phosphorylation pathway of chemoattraction

A

Empty receptor –> CheA –> CheY –> FliM –> tumble.

130
Q

CheA

A

Histidine kinase in chemoattraction pathway

131
Q

CheW

A

Highly conserved scaffold protein in chemoattraction pathway. Possibly not just a static role

132
Q

Methylation pathway of chemoattraction

A

CheR constitutively methylates. Methylated MCP has low affinity for substrate –> phosphorylation pathway –> tumbles.
CheA –> CheB –> demethylates MCP –> fewer tumbles.

133
Q

Bacterial adhesion

A

Binding host cells.
Pedestal formation.
Biofilms.
Intracellular.

134
Q

Bacterial binding host cells

A

Afimbrial adhesins, pili.

135
Q

Bacterial pili for adhesion

A

Type I, Type IV, Chaperone usher, Curli pili.

136
Q

Pedestals - topics to cover.

A 
Basic intro.
LEE and T3SS
Tir cascade. 
Actin polymerisation.
Other proteins injected.
137
Q

Types of afimbrial adhesin

A

E. coli NFA and AFA. Key in diffusely adhering E. coli. Bind DAF or CEA

138
Q

Delivery to sec pathway

A

Posttranslational: subunit made, signal recognized by SecB and delivered to periplasm by SecYEG due to ATPase activity of SecA.
Co-translational: delivered to SecA by FtsY.

139
Q

Bacteria using Type 1 pilus for adhesion.

A

Enterobacter.

140
Q

Bacteria using type 4 pili for adhesion.

A

Neisseria, Vibrio, Pseudomonas

141
Q

Type 4 pilin subunits. Tip adhesins.

A

P. Aeruginosa tip adhesin PilY1 binds asialoGM1/2

Neisseria tip adhesin binds CD46

142
Q

Type 4 pilin subunits. Major pilus subunit.

A

PilA

143
Q

Type 4 pili Base of structure

A

Inner membrane protein, channel in OM. Proteins to energise assembly.

144
Q

Type 4 pili channel in OM

A

PilQ

145
Q

Type 4 pili essential inner membrane protein

A

PilC

146
Q

Type 4 pili - PilB

A

Energises assembly via hydrolysis of NTPs.

147
Q

Type 4 pili - PilT

A

Energises retractiona and recycling of pilins.

148
Q

Type 4 pili - PilD

A

Specific peptidase on inner membrane, cleaves signal peptide for Sec pathway on secreted proteins.

149
Q

Type 4 pili - Neisseria.

A

Pilins are required for pathogenesis.

150
Q

Chaperone-usher pili in UPEC

A

P-pili and S-pili.

151
Q

Chaperone usher pili tropism

A

Most bacteria have more than one system, so tropism for many hosts.
Type 1 vs P-pili determines UPEC tropism

152
Q

Chaperone usher pili - type 1 pili

A

Leads to cystitis. Binds a-D-mannose in bladder.

Binding induces exfoliation, reveals lower layers which FimH also binds, promoting survival.

153
Q

Chaperone-usher pili - P-pili

A

Pyelonephritis. Binds Gal-a(1-4)-Gal. In kidney.

154
Q

P-pili proteins. Adhesin

A

PapG

155
Q

P-pili proteins. Order.

A

PapG to PapF to PapE (main component fibrillum) to PapK to PapA (main component of rod) to outer membrane usher, PapC.

156
Q

P-pili proteins. Periplasmic chaperone.

A

PapD

157
Q

P-pili proteins. Main pilus subunit.

A

PapA. Winds in right-handed helix.

158
Q

P-pili proteins. Growth terminator.

A

PapH terminates growth. Groove lacks pocket P5 necessary for donor strand exchange.

159
Q

P-pili proteins. PapE.

A

Main component fibrillum. Open helix configuration.

160
Q

P-pili proteins. PapK.

A

Links fibrillum to rod.

161
Q

P-pili proteins. Adhesin structure.

A

2 subdomains – N terminal mannose binding site - lectin domain; B-barrel jelly roll fold, but otherwise differing binding sites. C-terminal pilin domain incorporates into structure

162
Q

Signalling for termination of pilus growth.

A

CpxP suppresses CpxA, which when active phosphorylates CpxR which represses pap genes.
CpxP can bind aggregated proteins in periplasm, preventing CpxA binding and so lifting repression.

163
Q

Curli pili - used by…

A

Used by E. coli

164
Q

Curli pili assembly

A

CsgA exported by SecYEG. Exported by csgG in OM. Polymerises onto distal end of of pilus, like amyloid protein polymerization.

165
Q

Polysaccharides used for adhesion.

A 
LPS N. gonorrhoeae
LOS N. meningitides
EPS Pseudomonas
PIA S. epidermidis
Alginate P. aeruginosa.
166
Q

Bordetella pertussis afimbrial adhesins

A

Tracheal colonisation factor
Pertactin
Filamentous haemagglutinin.

167
Q

Pedestal formation - bacteria

A

EPEC and EHEC

168
Q

Pedestal formation

A

Locus of enterocyte effacement (LEE) codes for type III secretion system, and effectors.

169
Q

Type III secretion system from LEE

A

EspB and EspD form channel in host membrane for others to enter by. Also rearrange brush border and cytoskeleton in effacement of microvilli

170
Q

LEE - Tir

A

translocated intimin receptor with hairpin loop configuration.

171
Q

intimin

A

Intimin is an autotransporter whose membrane B-barrels bind each other, causing oligomerisation, and whose D2 and D3 domains bind Tir.

172
Q

EHEC Tir cascade

A

EspFu cascade

173
Q

EHEC Tir cascade details

A

Tir binds I-BAR which binds EspFu, which binds N-WASP, which binds Arp2/3, which causes actin polymerisation.

174
Q

EHEC - I-BAR

A

I-BAR has SH3 domain which binds EspFu. No direct contact between Tir and EspFu.
This must be BAR proteins key role because Tir-EspFu fusion protein rescues BAR deletion. May also have a role in membrane deformation.

175
Q

EPEC - Tir cascade.

A

Tir clustering leads to phosphorylation, binds Nck, binds N-WASP, binds Arp2/3, causes actin polymerisation.

176
Q

EPEC - Tir phosphorylation.

A

Tir clustering causes phosphorylation by host cell kinases such as c-Fyn (in membrane microdomains; initial burst of phosphorylation) and c-Abl at more than one site, but especially Y474P. Other kinases act to maintain.

177
Q

Arp2/3

A

Only Arp2/3 generates branched filamentous actin. Inactive alone - depends on nucleation promoting factors such as the WASP family.

178
Q

N-WASP

A

WCA nucleation promoting domain is sequestered by the GBD and PRD domains. Proteins that interact with these prevent this sequestration and cause activation.

179
Q

N-WASP interactions in Tir cascade.

A

Nck proteins interact with the PRD domain. EspFu binds AI domain (similar role). EspFu binds GBD using its CTD repeat region.

180
Q

LEE effector proteins - disrupting actin cytoskeleton

A

EspB and EspD

181
Q

Endocytic proteins recruited to pedestals

A

o Clathrin
o Clathrin adapter proteins.
o Dynamin
o BAR domain proteins

182
Q

LEE effector proteins - disruption of microtubules

A

EspG.

183
Q

Chaperone usher. Donor strand complementation. Subunit structure.

A

Incomplete Ig-like fold. Lack strand G of the 7 strand domain – hydrophobic groove. Causes misfolding.

184
Q

Chaperone usher. Donor strand complementation - process.

A

Chaperones have 2 domains, and insert their G1 into the subunit in a parallel manner to stabilise it. 4 pockets occupied, 5th is accessible for polymerisation.

185
Q

Chaperone usher. Donor strand exchange.

A

Usher displaces chaperone from acceptor subunit and replaces it with N-terminal extension of incoming subunit. Ntes insert into hydrophobic grooves with incredibly strong associations, using progressive displacement from P5 to P2.
Catalysed by usher, probably via proximity.

186
Q

Subunit ordering in chaperone-usher assembly.

A

First subunits have highest affinities for NTD compared to C-terminal domain. After that due to preference of subunits to polymerise with the correcct neighbour due to fit of P5 residue and P5 domain.

187
Q

Chaperone usher system; activation of the usher.

A

Plug domain displaced by lectin domain from incoming subunit.
Concomitantly changes from kidney shaped lumen to circular lumen.

188
Q

Listeria - regulation of virulence genes

A

Temperature change to 37 degrees –> conformational change in mRNA of PrfA –> can be translated –> makes PrfA –> activates small chromosomal pathogenicity island.

189
Q

TrxSR two component system

A

Widespread gene expression changes in response to ASN signalling. Including streptolysin toxin production.

190
Q

RNAIII structure - activity as riboregulator

A

Highly conserved 3’ domain important.
Has 14 stem loops.
Regulate hla positively , but others negatively, including rot, repressor of toxins.

191
Q

RNAIII translation

A

Gives d-hemolysin, which lysis cells by targetting membranes.

192
Q

CAI-1 and CqsS

A

Inhibits autophosphorylation

193
Q

Qrr effect on AphA

A

Qrr sRNAs cause it to adopt a conformation allowing translation.

194
Q

V. cholerae: virulence and QS

A

Virulence genes expressed at low cell density

195
Q

V. cholerae: biofilm and QS

A

Biofilm activated at low cell density.

ZZPathology undergraduate year 3, first term. (15 decks)

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