Abstract
Wolbachia pipientis is a ubiquitous, maternally transmitted bacterium that infects the germline of insect hosts. Estimates are that Wolbachia infect nearly 40% of insect species on the planet, making it the most prevalent infection on Earth. The bacterium, infamous for the reproductive phenotypes it induces in arthropod hosts, has risen to recent prominence due to its use in vector control. Wolbachia infection prevents the colonization of vectors by RNA viruses, including Drosophila C virus and important human pathogens such as Dengue and Chikungunya. Here we present data indicating that Wolbachia utilize the host actin cytoskeleton during oogenesis for persistence within and transmission between Drosophila melanogaster generations. We show that phenotypically wild type flies heterozygous for cytoskeletal mutations in Drosophila profilin (chic221/+ and chic1320/+) or villin (qua6-396/+) either clear a Wolbachia infection, or result in significantly reduced infection levels. This reduction of Wolbachia is supported by PCR evidence, Western blot results and cytological examination. This phenotype is unlikely to be the result of maternal loading defects, defects in oocyte polarization, or germline stem cell proliferation, as the flies are phenotypically wild type in egg size, shape, and number. Importantly, however, heterozygous mutant flies exhibit decreased total G-actin in the ovary, compared to control flies and chic221 heterozygous mutants exhibit decreased expression of profilin. Additionally, RNAi knockdown of profilin during development decreases Wolbachia titers. We analyze evidence in support of alternative theories to explain this Wolbachia phenotype and conclude that our results support the hypothesis that Wolbachia utilize the actin skeleton for efficient transmission and maintenance within Drosophila.
Highlights
Wolbachia pipientis is an intracellular α-proteobacterium that forms symbioses with an extremely broad array of hosts, including isopods, nematodes, and insects [1]
We show that phenotypically wild type flies heterozygous for cytoskeletal mutations in Drosophila profilin or villin either clear a Wolbachia infection, or result in significantly reduced infection levels
We show that after only two generations in a phenotypically wild type, heterozygous mutant fly, Wolbachia infections are cleared or reduced in titer
Summary
Wolbachia pipientis is an intracellular α-proteobacterium that forms symbioses with an extremely broad array of hosts, including isopods, nematodes, and insects [1]. Wolbachia are well known for the reproductive effects induced in the host, which range from the exotic (male killing) to the most common of reproductive effects, cytoplasmic incompatibility (CI) [1]. This recalcitrant, obligate symbiont has received much attention recently due to medical relevance. Wolbachia are heavily studied as potential drug targets for filarial nematode infection [3,4] and are currently being implemented to prevent transmission of Dengue fever from mosquitoes to humans [5,6]. Given the ubiquity of Wolbachia in the insect world, and its relevance to human health, it is essential to understand the biological basis of transmission of the symbiont between host generations
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