Wolinella succinogenes   Genome Project

The current understanding of bacterial pathogenicity mechanisms is largely based on the knowledge of the genomic inventory that is being shared by the most serious bacterial agents. Since many of these pathogenic organisms are strictly host-adapted their genomes have undergone a degrading process leading to small, minimalist genomes.

This process of deleting genetic information has resulted in orphaned cellular processes that can only be understood in their ancestral context. Such, to extend our knowledge on the origin and the emergence of a pathogen, it is essential to analyze the genomic inventory of living relatives with non-degraded genomes that have largely maintained the gene pool of a last common ancestor.

Members of the group of Helicobacteraceae and Campylobacteraceae are widespread pathogens, which in case of Helicobacter pylori and Campylobacter jejuni have been shown to colonize more than half of the human population, while Helicobacter hepaticus is specific to rodents.
C. jejuni is furthermore capable to colonize avians as a natural reservoir. In contrast to their pathogenic relatives, the rumen dweller W. succinogenes is the only member of the family of Campylobacterales, which is being considered to be non-pathogenic towards its mammalian host.

In our comparative genomic analysis we identify genes from a common shared ancestral gene pool that are essential for their maintenance in mammalian hosts, as well as species specific genes that may mediate the host and tissue specificity.

The adaptation to a specific niche or host is predicted to accelerate the gene loss of an organism. The observation that W. succinogenes does have a 450 kb larger genome than its pathogenic relatives is indicative of an organism that may be capable of living in the free environment.
This view is reinforcedby the fact that W. succinogenes not only has the most complete metabolism of all epsilon-proteobacteria studied so far, but also has extended capabilities of sensing environmental clues, as is evident from its numerous two-component signaling modules. The presence of a complete cluster of nitrogen fixation genes (nif) further may extend its biological fitness for growth in the environment by making it independent of nitrogen containing substrates.
Since many of the two-component signaling components, as well as the nifgene cluster show a high homology to genes found in cyanobacteria, W. succinogenes must have shared its ecological niche with these type of bacteria.

Thus we can demonstrate that studying environmental strains or closely related species of human pathogens results in an understanding of many "orphaned" processes in the metabolism and the signaling circuitry of an organism. Examples for this are truncated pathways of an oxidative metabolism in W. succinogenes and signaling cascades in H. pylori that are missing "up-stream" components, which are still present in W. succinogenes.

We therefore believe it is rewarding to re-assemble the complete set of physiological capabilities of the last common ancestor of this group of bacteria in order to draw conclusions on the emergence of their pathogenic interaction with a host.

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