Genomic Evolution of the Pathogenic Wolbachia Strain, wMelPop

Abstract

Most strains of the widespread endosymbiotic bacterium Wolbachia pipientis are benign or behave as reproductive parasites. The pathogenic strain wMelPop is a striking exception, however: it overreplicates in its insect hosts and causes severe life shortening. The mechanism of this pathogenesis is currently unknown. We have sequenced the genomes of three variants of wMelPop and of the closely related nonpathogenic strain wMelCS. We show that the genomes of wMelCS and wMelPop appear to be identical in the nonrepeat regions of the genome and differ detectably only by the triplication of a 19-kb region that is unlikely to be associated with life shortening, demonstrating that dramatic differences in the host phenotype caused by this endosymbiont may be the result of only minor genetic changes. We also compare the genomes of the original wMelPop strain from Drosophila melanogaster and two sequential derivatives, wMelPop-CLA and wMelPop-PGYP. To develop wMelPop as a novel biocontrol agent, it was first transinfected into and passaged in mosquito cell lines for approximately 3.5 years, generating wMelPop-CLA. This cell line-passaged strain was then transinfected into Aedes aegypti mosquitoes, creating wMelPop-PGYP, which was sequenced after 4 years in the insect host. We observe a rapid burst of genomic changes during cell line passaging, but no further mutations were detected after transinfection into mosquitoes, indicating either that host preadaptation had occurred in cell lines, that cell lines are a more selectively permissive environment than animal hosts, or both. Our results provide valuable data on the rates of genomic and phenotypic change in Wolbachia associated with host shifts over short time scales.

The transcriptome of the mosquito Aedes fluviatilis (Diptera: Culicidae), and transcriptional changes associated with its native Wolbachia infection

“…A further group of contigs included Wolbachia membrane proteins, and ankyrin genes, which are used to attach the bacterial membrane to the host cytoskeleton. These genes likely represent part of the machinery used to mediate Wolbachia -host interactions [39], are typically present in large numbers in Wolbachia genomes [35, 38, 40–42], and may also be involved in CI [43]. …”

Stability of the wMel Wolbachia Infection following Invasion into Aedes aegypti Populations

“…However there has been little change in cytoplasmic incompatibility caused by the infection or infection frequency in natural infected populations where a combination of maternal transmission leakage and cytoplasmic incompatibility dictates the expected frequency of the infection [7]. Moreover, genomic data point to little change in the w MelPop infection across 4 years after transfer into A. aegypti mosquitoes [8].…”

Drosophila melanogaster brain invasion: pathogenic Wolbachia in central nervous system of the fly

“…Opposite to mentioned benefit, Wolbachia laboratory strain wMelPop, accidently obtained by irradiation of males during the early study of Hannah (1949), has an exceptional ability to shorten the lifespan of a host, causing severe nerve and muscle tissue degeneration (Min & Benzer, 1997). Recently it was shown that the amplification of a specific region in wMelPop genome might be the reason of its strong pathogenic phenotype (Chrostek et al, 2013;Woolfit et al, 2013). Its rapid over-replication within the host tissues, especially in the brain, makes this strain unique, attractable to scientists and very promising candidate for biological control.…”