HspR and HrcA role in Helicobacter pylori heat-shock response

The ability of pathogens to perceive environmental conditions and modulate gene expression accordingly is a crucial feature for bacterial survival. In this respect, the heat-shock response allows cells to adapt to hostile environmental conditions and to survive during stress. In the major human pathogen Helicobacter pylori the expression of chaperone-encoding operons is under control of two auto-regulated transcriptional repressors, HrcA and HspR, with the latter acting as the master regulator of the regulatory circuit. To deepen our understanding of heat shock response in H. pylori and to further characterize the HspR regulon, we used global transcriptome analysis (RNA-sequencing) in combination with Chromatin Immunoprecipitation coupled with deep sequencing (ChIP-sequencing) of HspR genomic binding sites. We also defined the HrcA regulon, comparing the transcriptome of the H.pylori G27 wild type strain to that of the isogenic hrcA-knockout strain by RNA-sequencing. Finally, we compared HrcA and HspR regulons.