Abstract
Wolbachia is a group of intracellular symbiotic bacteria that widely infect arthropods and nematodes. Wolbachia infection can regulate host reproduction with the most common phenotype in insects being cytoplasmic incompatibility (CI), which results in embryonic lethality when uninfected eggs fertilized with sperms from infected males. This suggests that CI-induced defects are mainly in paternal side. However, whether Wolbachia-induced metabolic changes play a role in the mechanism of paternal-linked defects in embryonic development is not known. In the current study, we first use untargeted metabolomics method with LC-MS to explore how Wolbachia infection influences the metabolite profiling of the insect hosts. The untargeted metabolomics revealed 414 potential differential metabolites between Wolbachia-infected and uninfected 1-day-old (1d) male flies. Most of the differential metabolites were significantly up-regulated due to Wolbachia infection. Thirty-four metabolic pathways such as carbohydrate, lipid and amino acid, and vitamin and cofactor metabolism were affected by Wolbachia infection. Then, we applied targeted metabolomics analysis with GC-MS and showed that Wolbachia infection resulted in an increased energy expenditure of the host by regulating glycometabolism and fatty acid catabolism, which was compensated by increased food uptake. Furthermore, overexpressing two acyl-CoA catabolism related genes, Dbi (coding for diazepam-binding inhibitor) or Mcad (coding for medium-chain acyl-CoA dehydrogenase), ubiquitously or specially in testes caused significantly decreased paternal-effect egg hatch rate. Oxidative stress and abnormal mitochondria induced by Wolbachia infection disrupted the formation of sperm nebenkern. These findings provide new insights into mechanisms of Wolbachia-induced paternal defects from metabolic phenotypes.
Highlights
Wolbachia are endosymbiotic bacteria that frequently infect arthropods and nematodes[1,2]
Wolbachia can manipulate the reproduction of their insect hosts to enhance their transmission through host populations
Cytoplasmic incompatibility (CI) is the most common phenotype induced by Wolbachia in insect hosts, which results in embryonic mortality when Wolbachia infected males cross with normal females
Summary
Wolbachia are endosymbiotic bacteria that frequently infect arthropods and nematodes[1,2]. They can influence host reproduction by various strategies. Cytoplasmic incompatibility (CI) is the most common phenotype induced by Wolbachia in insect hosts, which causes lethality of embryos derived from the crosses between Wolbachia infected males and either uninfected females or females carrying a different strain of Wolbachia. When the Wolbachiainfected males mate with females infected with the same strain of Wolbachia, their offsprings develop properly[1,3,4]. The fact that Wolbachiainfected male insects caused no or few progenies when mated with uninfected females suggests that Wolbachia might induce paternal defects in embryonic development in insect hosts
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