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- W2794328591 abstract "Integration of horizontally acquired genes into transcriptional networks is essential for the regulated expression of virulence in bacterial pathogens. In Salmonella enterica, expression of such genes is repressed by the nucleoid-associated protein H-NS, which recognizes and binds to AT-rich DNA. H-NS-mediated silencing must be countered by other DNA-binding proteins to allow expression under appropriate conditions. Some genes that can be transcribed by RNA polymerase (RNAP) associated with the alternative sigma factor σS or the housekeeping sigma factor σ70 in vitro appear to be preferentially transcribed by σS in the presence of H-NS, suggesting that σS may act as a counter-silencer. To determine whether σS directly counters H-NS-mediated silencing and whether co-regulation by H-NS accounts for the σS selectivity of certain promoters, we examined the csgBA operon, which is required for curli fimbriae expression and is known to be regulated by both H-NS and σS . Using genetics and in vitro biochemical analyses, we found that σS is not directly required for csgBA transcription, but rather up-regulates csgBA via an indirect upstream mechanism. Instead, the biofilm master regulator CsgD directly counter-silences the csgBA promoter by altering the DNA-protein complex structure to disrupt H-NS-mediated silencing in addition to directing the binding of RNAP." @default.
- W2794328591 created "2018-03-29" @default.
- W2794328591 creator A5023026556 @default.
- W2794328591 creator A5032355641 @default.
- W2794328591 creator A5058310459 @default.
- W2794328591 creator A5083971720 @default.
- W2794328591 date "2018-02-20" @default.
- W2794328591 modified "2023-10-15" @default.
- W2794328591 title "The curli regulator CsgD mediates stationary phase counter‐silencing of <i>csgBA</i> in <i>Salmonella</i> Typhimurium" @default.
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- W2794328591 doi "https://doi.org/10.1111/mmi.13919" @default.
- W2794328591 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5867262" @default.
- W2794328591 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/29388265" @default.
- W2794328591 hasPublicationYear "2018" @default.
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