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The Complete Genome Sequence of the Murine Pathobiont Helicobacter typhlonius. | LitMetric

AI Article Synopsis

  • Researchers used immuno-compromised mice infected with Helicobacter typhlonius to study how it causes inflammatory bowel disease (IBD), leading to the sequencing of its complete genome.
  • The genome, which is 1.92 Mbp in size, includes 2,117 protein-encoding genes and shows significant similarity to H. hepaticus, indicating potential pathogenic features such as a type IV secretion system.
  • The findings, including the identification of unique methylation patterns, suggest that H. typhlonius may act as a pathogen, and further studies are needed to understand its full role in enteric diseases.

Article Abstract

Background: Immuno-compromised mice infected with Helicobacter typhlonius are used to model microbially inducted inflammatory bowel disease (IBD). The specific mechanism through which H. typhlonius induces and promotes IBD is not fully understood. Access to the genome sequence is essential to examine emergent properties of this organism, such as its pathogenicity. To this end, we present the complete genome sequence of H. typhlonius MIT 97-6810, obtained through single-molecule real-time sequencing.

Results: The genome was assembled into a single circularized contig measuring 1.92 Mbp with an average GC content of 38.8%. In total 2,117 protein-encoding genes and 43 RNA genes were identified. Numerous pathogenic features were found, including a putative pathogenicity island (PAIs) containing components of type IV secretion system, virulence-associated proteins and cag PAI protein. We compared the genome of H. typhlonius to those of the murine pathobiont H. hepaticus and human pathobiont H. pylori. H. typhlonius resembles H. hepaticus most with 1,594 (75.3%) of its genes being orthologous to genes in H. hepaticus. Determination of the global methylation state revealed eight distinct recognition motifs for adenine and cytosine methylation. H. typhlonius shares four of its recognition motifs with H. pylori.

Conclusion: The complete genome sequence of H. typhlonius MIT 97-6810 enabled us to identify many pathogenic features suggesting that H. typhlonius can act as a pathogen. Follow-up studies are necessary to evaluate the true nature of its pathogenic capabilities. We found many methylated sites and a plethora of restriction-modification systems. The genome, together with the methylome, will provide an essential resource for future studies investigating gene regulation, host interaction and pathogenicity of H. typhlonius. In turn, this work can contribute to unraveling the role of Helicobacter in enteric disease.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4705304PMC
http://dx.doi.org/10.3389/fmicb.2015.01549DOI Listing

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