科研之友
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摘要
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. @@@ Author summary Wolbachia are among the most successful intracellular bacteria that can infect many arthropod species as well as filarial nematodes. 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 (uninfected) females. This indicates that the impact of Wolbachia infection is mainly on paternal side. Evidence has suggested that the metabolism is strongly linked with male reproduction. We were interested in investigating whether Wolbachia-induced metabolic changes involve in the mechanism of paternal defects in embryogenesis. Here, using comparative metabolomics method, we identified 414 potential differential metabolites related to 34 metabolic pathways between Wolbachia-bearing and Wolbachia-free male Drosophila melanogaster. Then, by targeted metabolomics analysis, gene overexpression, and transmission electron microscopy (TEM) techniques, we found that in Wolbachia infected D. melanogaster, energy metabolism and oxidative stress were enhanced, and the development of mitochondria-derived nebenkern during spermatogenesis was impaired. These may be the main causes of paternal defects induced by Wolbachia.
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单位中国科学院; 中国科学院研究生院
