Role of RNase J in the regulation of RNA stability in the gastric pathogen Helicobacter pylori

Stomach colonisation by the important human pathogen Helicobacter pylori (Hp) requires specific adaptation strategies to the highly acidic environment of the stomach. The bacterial response to the gastric environment involves several levels of control including post-transcriptional regulation of gene expression. We investigate the importance of such a regulation in Hp specifically at the level of RNA stability. RNase E is absent from the genome of Hp but the homolog of the Bacillus subtilis RNase J1 is both conserved and essential in Hp (gene hp1430, Hp-RNase J). To investigate the role of Hp-RNase J in vivo, we constructed an Hp B128 strain that expresses gene hp1430 under control of an inducible promoter and permits depletion of the Hp-RNase J protein level. The strain displays important growth retardation and more than five-fold decrease in the Hp-RNase J protein level in the absence of inducer. Hp-RNase J depletion leads to the stabilisation of its own mRNA, not detectable in the wild type strain, suggesting that the gene encoding Hp-RNase J is subject to autoregulation. To investigate the global impact of Hp-RNase J on the Hp RNA metabolism, we used the high throughput sequencing technology of Solexa to sequence the total RNAs isolated from the Hp strain depleted or not for Hp-RNase J. In average, about 58 million of reads were obtained per sample that aligned to the H. pylori B128 genome. The analysis of the data is in progress.