Transcriptome Complexity and Riboregulation in the Human Pathogen Helicobacter pylori

Abstract

The Gram-negative Epsilonproteobacterium Helicobacter pylori is considered as one of the major human pathogens and many studies have focused on its virulence mechanisms as well as genomic diversity. In contrast, only very little is known about post-transcriptional regulation and small regulatory RNAs (sRNAs) in this spiral-shaped microaerophilic bacterium. Considering the absence of the common RNA chaperone Hfq, which is a key-player in post-transcriptional regulation in enterobacteria, H. pylori was even regarded as an organism without riboregulation. However, analysis of the H. pylori primary transcriptome using RNA-seq revealed a very complex transcriptional output from its small genome. Furthermore, the identification of a wealth of sRNAs as well as massive antisense transcription indicates that H. pylori uses riboregulation for its gene expression control. The ongoing functional characterization of sRNAs along with the identification of associated RNA binding proteins will help to understand their potential roles in Helicobacter virulence and stress response. Moreover, research on riboregulation in H. pylori will provide new insights into its virulence mechanisms and will also help to shed light on post-transcriptional regulation in other Epsilonproteobacteria, including widespread and emerging pathogens such as Campylobacter.

A variable homopolymeric G-repeat defines small RNA-mediated posttranscriptional regulation of a chemotaxis receptor in Helicobacter pylori

“…The length of this G-repeat varies among different Helicobacter strains and thereby determines sRNA-mediated translational repression or activation and strain-specific regulation. must act independently of Hfq and their study will provide new insights into mechanisms of sRNA-mediated regulation and virulence control (22).…”

The Family Helicobacteraceae

“…The H. pylori transcriptome is a very complex and compact structure (Sharma et al 2010) comprising massive antisense transcription, with more than 60 small RNAs (sRNAs) and potential regulators of cis and transcoded mRNA targets. It has been proposed that H. pylori uses riboregulation for control of its gene expression (Pernitzch and Sharma 2012). Small hydrophobic proteins may also participate in the transcription regulation (Pernitzch and Sharma 2012).…”

“…It has been proposed that H. pylori uses riboregulation for control of its gene expression (Pernitzch and Sharma 2012). Small hydrophobic proteins may also participate in the transcription regulation (Pernitzch and Sharma 2012). H. pylori contains several RNases, including RNase H, RNase H-II, RNase J, RNase N, RNase P, RNase R and RNase III, but as observed in all Epsilonproteobacteria, it lacks RNase E. RNase J and RNase III are thought to regulate virulence related genes (Tsao et al 2009), reviewed in (Pernitzch and Sharma 2012).…”

“…Small hydrophobic proteins may also participate in the transcription regulation (Pernitzch and Sharma 2012). H. pylori contains several RNases, including RNase H, RNase H-II, RNase J, RNase N, RNase P, RNase R and RNase III, but as observed in all Epsilonproteobacteria, it lacks RNase E. RNase J and RNase III are thought to regulate virulence related genes (Tsao et al 2009), reviewed in (Pernitzch and Sharma 2012). Cytosine methylation of H. pylori DNA may also modulate the expression of virulence factors by inhibiting genes that encode OMPs, CagA, VacA and genes controlling motility .…”

Cooperation of Gastric Mononuclear Phagocytes with Helicobacter pylori during Colonization

“…Helicobacter pylori is a microaerophilic, Gram-negative, spiral-shaped bacterium that selectively establishes lifelong colonization of the gastric mucosa in over 50% of the human population (1, 2). Approximately 10–15% of H. pylori -infected individuals will eventually develop gastro-duodenal ulcers and H. pylori carriers have over a two-fold greater risk of developing gastric cancer in the form of B-cell lymphoma of mucosal-associated lymphoid tissue (MALT) lymphoma or adenocarcinoma (3, 4).…”