Genome expansion of an obligate parthenogenesis-associated Wolbachia poses an exception to the symbiont reduction model

Kampfraath AA, Klasson L, Anvar SY, Vossen RHAM, Roelofs D, Kraaijeveld K, Ellers J

BMC Genomics 20 (1) 106 [2019-12-00; online 2019-02-06]

Theory predicts that dependency within host-endosymbiont interactions results in endosymbiont genome size reduction. Unexpectedly, the largest Wolbachia genome was found in the obligate, parthenogenesis-associated wFol. In this study, we investigate possible processes underlying this genome expansion by comparing a re-annotated wFol genome to other Wolbachia genomes. In addition, we also search for candidate genes related to parthenogenesis induction (PI). Within wFol, we found five phage WO regions representing 25.4% of the complete genome, few pseudogenized genes, and an expansion of DNA-repair genes in comparison to other Wolbachia. These signs of genome conservation were mirrored in the wFol host, the springtail F. candida, which also had an expanded DNA-repair gene family and many horizontally transferred genes. Across all Wolbachia genomes, there was a strong correlation between gene numbers of Wolbachia strains and their hosts. In order to identify genes with a potential link to PI, we assembled the genome of an additional PI strain, wLcla. Comparisons between four PI Wolbachia, including wFol and wLcla, and fourteen non-PI Wolbachia yielded a small set of potential candidate genes for further investigation. The strong similarities in genome content of wFol and its host, as well as the correlation between host and Wolbachia gene numbers suggest that there may be some form of convergent evolution between endosymbiont and host genomes. If such convergent evolution would be strong enough to overcome the evolutionary forces causing genome reduction, it would enable expanded genomes within long-term obligate endosymbionts.

Bioinformatics Support for Computational Resources [Service]

NGI Uppsala (Uppsala Genome Center) [Service]

National Genomics Infrastructure [Service]

PubMed 30727958

DOI 10.1186/s12864-019-5492-9

Crossref 10.1186/s12864-019-5492-9

pii: 10.1186/s12864-019-5492-9
pmc: PMC6364476