Global Gene Expression and Phenotypic Analysis of a Vibrio cholerae rpoH Deletion Mutant

Vibrio cholerae, the cause of cholera, can grow in a variety of environments outside of human hosts. During infection, this pathogen must adapt to significant environmental alterations, including the elevated temperature of the human gastrointestinal tract. σ32, an alternative sigma factor encoded by rpoH, activates transcription of genes involved in the heat shock response in several bacterial species. Here, we assessed the role of σ32 in V. cholerae physiology. In aggregate, our findings suggest that σ32 promotes V. cholerae growth at temperatures ranging at least from 15°C to 42°C. Growth of the rpoH mutant was severely attenuated within the suckling mouse intestine, suggesting that σ32-regulated genes are critical for V. cholerae adaptation to conditions within the gastrointestinal tract. We defined the V. cholerae RpoH regulon by comparing the whole-genome transcription profiles of the wild-type and rpoH mutant strains after a temperature up-shift. Most of the V. cholerae genes expressed in an RpoH-dependent manner after heat shock encode proteins that influence protein fate, such as proteases and chaperones, or are of unknown function. Bioinformatic analyses of the microarray data were used to define a putative σ32 consensus binding sequence and subsequently to identify genes that are likely to be directly regulated by RpoH in the whole V. cholerae genome.