Abstract
Although successful and persistent colonization of the gastric mucosa depends on the ability to respond to changing environmental conditions and co-ordinate the expression of virulence factors during the course of infection, Helicobacter pylori possesses relatively few transcriptional regulators. Among these regulators csrA ( carbon storage regulator; locus tag:HP1442; GI:15646051) was necessary for full motility and survival of H. pylori under conditions of oxidative stress. Loss of csrA expression deregulated the oxidant-induced transcriptional responses of napA and ahpC, the acid induction of napA, cagA, vacA, the urease operon, and fur, as well as the heat shock responses of napA, groESL and hspR. Finally, H. pylori strains deficient in the production of CsrA were significantly attenuated for virulence in a mouse model of infection. Therefore, csrA has a broad role in regulating the physiology of H. pylori in response to environment stimuli. Deeply to say, CsrA appear to mediate its effect in H. pylori at the post-transcriptional level by influencing the processing and translation of target transcripts, with minimal effect on the stability of the target mRNAs. In order to find out the mechanism of mRNA binding, we use NMR spectroscopy to determine the solution structure of HP1442 and attempt to propose the crucial residues for specificity.