Comparative Genomics of a Parthenogenesis-Inducing Wolbachia Symbiont.

Wolbachia is an intracellular symbiont of invertebrates responsible for inducing a wide variety of phenotypes in its host. These host-Wolbachia relationships span the continuum from reproductive parasitism to obligate mutualism, and provide a unique system to study genomic changes associated with the evolution of symbiosis. We present the genome sequence from a parthenogenesis-inducing Wolbachia strain (wTpre) infecting the minute parasitoid wasp Trichogramma pretiosum The wTpre genome is the most complete parthenogenesis-inducing Wolbachia genome available to date. We used comparative genomics across 16 Wolbachia strains, representing five supergroups, to identify a core Wolbachia genome of 496 sets of orthologous genes. Only 14 of these sets are unique to Wolbachia when compared to other bacteria from the Rickettsiales. We show that the B supergroup of Wolbachia, of which wTpre is a member, contains a significantly higher number of ankyrin repeat-containing genes than other supergroups. In the wTpre genome, there is evidence for truncation of the protein coding sequences in 20% of ORFs, mostly as a result of frameshift mutations. The wTpre strain represents a conversion from cytoplasmic incompatibility to a parthenogenesis-inducing lifestyle, and is required for reproduction in the Trichogramma host it infects. We hypothesize that the large number of coding frame truncations has accompanied the change in reproductive mode of the wTpre strain

Evolutionary Genetics of Microbial Symbiosis

Symbiosis is the living together of dissimilar organisms [1,2]. As such, symbiotic relationships can range from antagonist (parasitic) to mutualistic and can vary along this continuum within and between species in space and time. Microbial symbioses encompass a wide array of players (e.g., bacteria, fungi, and small eukaryotes) and are an integral part of organismal life, contributing to phenotypes at all levels of biological organization, from molecules to ecosystems. There has been an explosion of microbiological research on symbiosis emerging from the omics revolution, which has made many previously intractable symbioses available for dissection. Current research ranges from unraveling the biochemical interactions among symbiont partners to uncovering the incredible ecological diversity and dynamics of microbial communities and host associations. Host-microbes engage in extensive and complex cross-kingdom molecular dialogue, where symbionts can modulate their reciprocal gene expression patterns, complement metabolic pathways, and combine genetic information through DNA exchange, in some cases becoming sufficiently integrated through coinheritance to be considered as an evolutionary unit of selection. This extensive genetic and biochemical interplay has enormous implications in the emergence of novel traits and the overall diversification of life

Accelerated microevolution in an outer membrane protein (OMP) of the intracellular bacteria Wolbachia

<p>Abstract</p> <p>Background</p> <p>Outer membrane proteins (OMPs) of Gram-negative bacteria are key players in the biology of bacterial-host interactions. However, while considerable attention has been given to OMPs of vertebrate pathogens, relatively little is known about the role of these proteins in bacteria that primarily infect invertebrates. One such OMP is found in the intracellular bacteria <it>Wolbachia</it>, which are widespread symbionts of arthropods and filarial nematodes. Recent experimental studies have shown that the <it>Wolbachia </it>surface protein (WSP) can trigger host immune responses and control cell death programming in humans, suggesting a key role of WSP for establishment and persistence of the symbiosis in arthropods.</p> <p>Results</p> <p>Here we performed an analysis of 515 unique alleles found in 831 <it>Wolbachia </it>isolates, to investigate WSP structure, microevolution and population genetics. WSP shows an eight-strand transmembrane β-barrel structure with four extracellular loops containing hypervariable regions (HVRs). A clustering approach based upon patterns of HVR haplotype diversity was used to group similar WSP sequences and to estimate the relative contribution of mutation and recombination during early stages of protein divergence. Results indicate that although point mutations generate most of the new protein haplotypes, recombination is a predominant force triggering diversity since the very first steps of protein evolution, causing at least 50% of the total amino acid variation observed in recently diverged proteins. Analysis of synonymous variants indicates that individual WSP protein types are subject to a very rapid turnover and that HVRs can accommodate a virtually unlimited repertoire of peptides. Overall distribution of WSP across hosts supports a non-random association of WSP with the host genus, although extensive horizontal transfer has occurred also in recent times.</p> <p>Conclusions</p> <p>In OMPs of vertebrate pathogens, large recombination impact, positive selection, reduced structural and compositional constraints, and extensive lateral gene transfer are considered hallmarks of evolution in response to the adaptive immune system. However, <it>Wolbachia </it>do not infect vertebrates. Here we predict that the rapid turnover of WSP loop motifs could aid in evading or inhibiting the invertebrate innate immune response. Overall, these features identify WSP as a strong candidate for future studies of host-<it>Wolbachia </it>interactions that affect establishment and persistence of this widespread endosymbiosis.</p

Genetic Incompatibilities Between Mitochondria and Nuclear Genes: Effect on Gene Flow and Speciation

The process of speciation is, according to the biological species concept, the reduction in gene flow between genetically diverging populations. Most of the previous theoretical studies analyzed the effect of nuclear genetic incompatibilities on gene flow. There is, however, an increasing number of empirical examples suggesting that cytoplasmically inherited genetic elements play an important role in speciation. Here, we present a theoretical analysis of mitochondrial driven speciation, in which genetic incompatibilities occur between mitochondrial haplotypes and nuclear alleles. Four population genetic models with mainland-island structure were analyzed that differ with respect to the type of incompatibility and the underlying genetics. Gene flow reduction was measured on selectively neutral alleles of an unlinked locus and quantified by the effective migration rate. Analytical formulae for the different scenarios were derived using the fitness graph method. For the models with haploid genetics, we found that mito-nuclear incompatibilities (MtNI) are as strong as nuclear-nuclear incompatibilities (NNI) in reducing gene flow at the unlinked locus, but only if males and females migrate in equal number. For models with diploid genetics, we found that MtNI reduce gene flow stronger than NNI when incompatibilities are recessive, but weaker when they are dominant. For both haploid and diploid MtNI, we found that gene flow reduction is stronger if females are the migrating sex, but weaker than NNI when males are the migrating sex. These results encourage further examination on the role of mitochondria on genetic divergence and speciation and point toward specific factors (e.g., migrating sex) that could be the focus of an empirical test