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SUMMARY:Exit from dormancy in bacteria 
DTSTART;VALUE=DATE:20101001
DTSTAMP:20260428T161451Z
UID:c85ee57c2a1cd62e507eed9384511022e1bf3189568f69345081a19c
CATEGORIES:Conferences - Seminars
DESCRIPTION:Jonathan Dworkin\, Columbia University\, NY\nBacteria can ente
 r a metabolically inactive state of dormancy that facilitates survival und
 er conditions unfavorable to growth and provide phenotypic resistance to m
 any anti-microbials. This state comes at a cost\, though\, as inactive cel
 ls run the risk of being outcompeted by their neighbors. The decision to h
 alt or reinitiate growth must therefore be carefully regulated. We have fo
 und that exit from dormancy (germination) in the spore-forming bacterium B
 acillus subtilis in response to peptidoglycan muropeptides is dependent on
  PrkC\, a eukaryotic-like Ser/Thr membrane kinase. Since muropeptides are 
 released by dividing bacteria\, their presence serves as a signal that the
  environment supports bacterial growth. We further found that early in ger
 mination\, the PrkC kinase phosphorylates Elongation Factor G (EF-G)\, the
  essential translation GTPase necessary for mRNA translocation. Since this
  kinase is broadly conserved\, phosphorylation of EF-G in non-growing cell
 s of diverse bacteria may stimulate their growth.
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STATUS:CONFIRMED
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