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SUMMARY:Redox signaling mechanisms under infection conditions and antibiot
 ics in the major pathogen Staphylococcus aureus
DTSTART:20191001T163000
DTEND:20191001T180000
DTSTAMP:20260427T200800Z
UID:1cd4e5e7d23541a737ee1ab96759482df624c819c1960340e2b70e5d
CATEGORIES:Conferences - Seminars
DESCRIPTION:Prof. Haike Antelmann\nStaphylococcus aureus has to cope with 
 reactive oxygen\, electrophile and chlorine species (ROS\, RES\, RCS) duri
 ng infections and antibiotics treatment. We are interested in redox signal
 ing and defense mechanisms of redox-active species\, such as HOCl\, quinon
 es and antibiotics in S. aureus. The Rrf2- family regulator HypR was descr
 ibed as novel redox-sensitive repressor that controls the flavin disulfide
  reductase MerA and directly senses and responds to HOCl\, diamide and all
 icin stress via a thiol-disulfide switch in S. aureus. MerA was shown to f
 unctions as disulfide reductase to protect S. aureus against HOCl and alli
 cin stress and increased survival in J774A.1 macrophage infection assays.\
 nIn addition\, the MarR-type regulator MhqR was identified as novel quinon
 e-sensing repressor of the mhqRED operon\, which is involved in quinone de
 toxification. The MhqR repressor is directly inactivated by quinones and l
 ikely binds to a specific quinone-binding pocket. In phenotypic assays\, t
 he mhqR deletion mutant was resistant to MHQ and quinone-like antimicrobia
 ls\, such as pyocyanin\, ciprofloxacin\, norfloxacin and rifampicin. Moreo
 ver\, the MhqR regulon contributes to an improved survival under lethal RO
 S and after long-term infections in S. aureus.\nApart from redox-sensing r
 egulators\, the low molecular weight thiol bacillithiol (BSH) plays an imp
 ortant role to maintain the thiol-redox homeostasis in S. aureus. Under HO
 Cl stress\, BSH forms mixed disulfides with proteins thiols\, termed as pr
 otein S-bacillithiolation to protect redox-sensitive thiols against overox
 idation and to regulate protein functions. The glycolytic glyceraldehyde-3
 - phosphate dehydrogenase GapDH and the aldehyde dehydrogenase AldA were d
 iscovered as most abundant targets for S-bacillithiolation in S. aureus. T
 he reversal of S-bacillithiolation is redox- controlled by the Brx/BSH/Ypd
 A pathway. Moreover\, the bacilliredoxin BrxA and the BSSB reductase YpdA 
 were shown to be essential under oxidative stress and infections condition
 s. In conclusion\, our studies discovered novel redox-regulators and impor
 tant thiol-switches that play essential role for survival under HOCl\, qui
 nones and infection conditions in S. aureus.
LOCATION:BCH 2201 https://plan.epfl.ch/?room==BCH%202201
STATUS:CONFIRMED
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