Rational design of an artificial genetic switch: Co-option of the H-NS-repressed proU operon by the VirB virulence master regulator.

ABSTRACT: The H-NS protein represses the transcription of hundreds of genes in Gram-negative bacteria. Derepression is achieved by a multitude of mechanisms, many of which involve the binding of a protein to DNA at the repressed promoter in a manner that compromises the maintenance of the H-NS-DNA nucleoprotein repression complex. The principal virulence gene promoters in Shigella flexneri, the cause of bacillary dysentery, are repressed by H-NS. VirB, a protein that closely resembles members of the ParB family of plasmid-partitioning proteins, derepresses the operons that encode the main structural components and the effector proteins of the S. flexneri type III secretion system. Bioinformatic analysis suggests that VirB has been co-opted into its current role as an H-NS antagonist in S. flexneri.

SUBMITTER: Kane KA 

PROVIDER: S-EPMC3194901 | biostudies-literature | 2011 Nov

REPOSITORIES: biostudies-literature