Subsystem: Persister Cells

This subsystem's description is:

Genes involved in the formation of persister cells, long-time survivors in stressed bacterial populations.

For more information, please check out the description and the additional notes tabs, below

Literature ReferencesBacterial persistence: some new insights into an old phenomenon. Jayaraman R Journal of biosciences 2008 Dec19179767
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HipAHipBRmfSulA
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Genes involved in the formation of persister cells, long-time survivors in stressed bacterial populations.
The entrance of cells into a dormant, persistent state is largely responsible for the multidrug tolerance of infections. Persisters in biofilms account for their tolerance to all known antimicrobials. Persisters are likely to be responsible for latent (chronic) diseases.
Persisters are different from antibiotic-resistant mutants in that their antibiotic tolerance is non-heritable and reversible.

Persistence is the end result of a stochastic switch in the expression of some toxin–antitoxin (TA) modules (like hipA/hipB), creating an imbalance in their intracellular levels. The toxin then inactivates the targets of antibiotics (ribosomes, cell wall synthesis, etc); therefore, the antibiotics can no longer corrupt them into malfunctioning, leading to antibiotic tolerance and the persister state.

This SS gathers some of the genes known from genetic studies to be relevant to the establishment of the persistent state. Other genes involved are the toxin-antitoxin loci.
Genes central to metabolism such as glycerol-3-phosphate dehydrogenase and glycerol-3-phosphate acyltransferase also affect entrance to the persistent state.