L12 - Regulation & Environmental Interactions Flashcards

1
Q

Bacteria mustadaptto changing environments to survive and successfully colonize hosts. Key aspects include:

A
  • Adjusting tonew environments
  • Evading host defenses through subversion or circumvention
  • Ensuring long-term survival
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2
Q

How does regulation allow bacteria to control survival phenotypes?

A

Tailoring needs to a specific niche– particularly within thehost environment, where the immune system actively prevents infection.

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3
Q

What is niche-dependent behaviour and what are some examples of niches shifts.

A
  • Example: Switching between attachment(to host cells) andavoidance (immune evasion).
  • Transitioning betweenintracellular andextracellular lifestyles.
  • encironment of host os constrictive
  • microbe has sensed niche change e.g. water in gut
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4
Q

What are some ways in which bacteria interact with the host?

A
  • Prevention of opsonization(avoiding immune detection).
  • Toxin secretion– neutralizes host defenses.
  • Disrupting mucosal integrity– facilitates infection.
  • Modifying microbial recognition– alteringPAMPs(Pathogen-Associated Molecular Patterns) to evade detection.
  • Chemokine interference– reduces immune response signaling.
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5
Q

How does infection occur and how do bacteria employ genetic strategies to enhance infecticity?

A
  • Plasmids– carry virulence genes.
  • Mobile genetic elements– includepathogenicity islands, which encode toxins and other factors.
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6
Q

How do bacteria sense their environment and regulate gene expression?

A
  • regulatory networks (detect host signals to control gene expression)
  • two-component systems (2CS) - sense environmental cues like magnesium levels temp and ph
  • quorum sensing adjusts biofilm formation and virulence based on population density
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7
Q

What are the 2 types of responses from gene expression

A

Transient - reversible, non- mutational gene expression changes

Constitutive - permanent, multinational adaptations

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8
Q

What are the diff membrane-associated signalling systems to regulate gene expression ?

A

One component system, two component system, anti-sigma factors

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9
Q

Give definitions :
- signal
- sensor
- regulator
- regulon
- positive or negative control
- housekeeping vs virulence genes

A
  • Signal– Environmental cue triggers gene regulation.
  • Sensor– Protein detects the signal, changes conformation.
  • Regulator– DNA-binding protein controls gene expression.
  • Regulon– Group of genes regulated together.
  • Positive or Negative Control– Genes can be activated or repressed.
  • Housekeeping vs. Virulence Genes– Some genes are always on (housekeeping), while virulence genes are regulated based on need.
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10
Q

Describe bacterial regulons

A

Many ‘house keeping’ genes formed into networked hierarchies

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11
Q

Describe the environmental regulation of 2CS in regards to stimulus response mechanism and gene regulation

A

Stimulus response mechanism = signal transduction phosphoration transcription protein by histidine kinase sensor

Gene regulation - interaction with transcription protein (activator or repressor) effects on RNA polymerase sigma factors and DNA binding regulator

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12
Q

What is the location of regulatory protein and sensor?

A

Regulatory protein in cytoplasm and sensor in membrane

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13
Q

Histidine protein kinase causes what ? 2c can not perform regulators without what?

A

Conformational change - autophosphorylation and cannot perform regulators without phosphate

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14
Q

Describe the model for regulation of PhoP/Pho in enterobacteriales

A

High Mg2+ system is off -

Low Mg2+ system is on and activation is triggered, responds to host-derived SMPs leading to resistance mechanisms.

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15
Q

What are the diff components in PhoQ/PhoR?

A

PhoQ is the sensor kinase and detects low Mg2+ levels or presence of AMPs. Phosphorylation itself and transfers phosphate to PhoP

PhoP is the response regulator and it controls expression of multiple genes regulating LPS modification, AMP resistance and virulence factors

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16
Q

Summary:
Adaptive response to ___ extra cellular Mg2+ conc is required for ____. PhoP-PhoQ modifies ___ and controls resistance to ___ and ____. Reduced microbial virulence and increased in vivo immune ____

A

Low, pathogenesis , LPS, polymyxin B, AMP, evasion

17
Q

What is a biofilm?

A

Structured community of bacterial cells enclosed in a self-produced polymeric matrix and adherent to an inert or living surface.

18
Q

What is quorum sensing in terms of regulatory mechanism

A

Cell population density dependent regulation mediated via self generated extracellular signal molecules (autoinducrs)

19
Q

How is biolfim used for bacterial self protection

A

Antibiotic only eradicated top most layer

20
Q

What are the different low weight inducer molecules in gram positive vs gram negative bactera in primary QS

A

Positive = autoinducing peptides (AIPs)
Negative = acrylic-homoserine lactose’s (AHLs)

21
Q

What is the structure of AHLs

A
  • homoserine lectone ring
  • Fatty acyl side chain(length and modifications vary among species)
22
Q

What is the process of AHL QS signaling

A
  1. Synthesis– AHLs are synthesized byLuxI-type enzymes.
  2. Diffusion– AHLs diffusefreely across the bacterial membrane.
  3. Accumulation– As bacterial density increases, AHLsbuild up in the environment.
  4. Detection– When AHLs reach a threshold, they bind toLuxR-type regulators.
  5. Gene Activation– The LuxR-AHL complex binds to DNA andactivates or represses target genes.
23
Q

What are the signal synthase and receptors in QS

A

LasRI or RhlRI

24
Q

What does QS regulate

A
  • biofilm formation, toxin production and virulence gene activation
25
Q

What are the different components in quorum sensing

A

Signal synthase (produces the autoinducers)
Signal receptor (detects signal molecules)
Autoinducers (small molecules that modulate gene expression)

26
Q

How is quorum sensing achieved in pseudomonas aeruginosa

A
  • UsesLasRI & RhlRIsystems to regulate virulence.
  • LuxR-type regulatorscontrol transcription.
  • QS influences host-pathogen interactions:
    • Induces pro-inflammatory cytokines.
    • Enhances immune cell chemotaxis.
    • Produces toxins (e.g., pyocyanin)that increase inflammation.
    • Attenuates LPS-induced inflammationto promote infection.