Regulation of Bacterial Processes and Environmental Interactions Flashcards
Describe how quorum sensing and two-component regulatory systems allow cells to adapt to fluctuating conditions.
quiz
Define the condition, if it is in vivo
Two component regulatory systems
-Discuss the PhoPQ system in Salmonella Typhimurium
-Include SPI-2 induction of T3SS release of effectors, LPS
modification and intramacrophage survival
Quorum sensing systems
-Discuss LasRI and RhlRI system in Pseudomonas aeruginosa
-Effect of the production of pyocyanin, exotoxin A
Can you think of more examples?
How do efflux pumps contribute to pathogenesis?
quiz
-Using the example of AcrAB-TolC system which is also a Type I secretion system involved in the extrusion of antibiotics and host defense factors
-Functional in both environmental and in vivo conditions
-Subject to regulation by multiple regulatory factors which are important for survival
How are bacterial virulence factors controlled?
quuiz
-Responsive, conditional or constitutive
-Provide examples T3SS expression-effector release QS systems, LPS modifications
How does bacterial gene regulation control virulence?
Environmental signals influence gene regulation, which can promote virulence factors. For example, when enterobacteria get eaten by a macrophage, the Mg and Ca levels drop which induces PhoP/PhoQ pathway which produces LPS.
LPS is virlence facotr, PhoP/PhoQ is a two component system
How do the gene regulatory circuits work in concert to facilitate colonisation and pathogenesis?
PhoP-PhoQ and PmrA-PmrB work in conjunction and act on the same regulon/overlapping regulons to modify LPS which leads to antimicrobial peptide resistance
How is gene expression managed at a community level (biofilm) to ensure in vivo survival?
Quorum sensing, and auto-inducer production
eg. AIP - gram pos and AHL- gram neg
LasR/Rh1r are set off when biofilms detect HSL which is an autoinducer (which makes toxins like pyomyacin which damages tissues)
Autoinducers are produced by all bacteria, and if theres a high conc of bacteriial cells then the conc of auto inducers is high enough to generate genetic cascade
Essentially, signals that biofilm is big enough to start becoming pathogenic
Why is sensing the environment relevant to bacterial colonisation and infection?
Change in conditions allows it to control what genes are expressed which allows it to survive in those conditions and optomize energy usage
Eg PhoP-PhoQ are activated when Mg is low
How can bacteria utilise these genetic systems to evade the immune response or cause pathogenesis?
Can use complement systems to produce toxins/set off genetic cascades
What are three things that two component regulatory systems do to contribute to pathogenicity?
- Trigger toxin production
- Trigger cellular damage
- Lipopolysaccaride modification