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A host–parasite interaction rescues Drosophila oogenesis defects

Abstract

The cytoplasmically inherited bacterium Wolbachia pipientis is a widespread parasite of arthropods that manipulates the reproductive biology of its hosts, often to their detriment, in order to foster its own transmission through egg cytoplasm1,2. Here we report that infection by Wolbachia restores fertility to Drosophila melanogaster mutant females prevented from making eggs by protein-coding lesions in Sex-lethal (Sxl), the master regulator of sex determination. Suppression of sterility by Wolbachia discriminates markedly among similar germline-specific Sxl alleles, and is not observed for mutations in other genes that produce similar ‘tumorous ovary’ phenotypes, including one that blocks Sxl germline expression. This allele and gene specificity indicates that suppression probably results from a specific interaction with Sxl protein, rather than from a bypass of the normal germline requirement for this developmental regulator or from an effect on Sxl expression. The SxlWolbachia interaction provides a rare opportunity to explore host–parasite relationships at the molecular level in a model insect. Furthermore, demonstration that a parasite infection can counteract the deleterious effects of mutations in host genes illustrates how hosts might become dependent on parasites.

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Figure 1: Egg production in Sxlf4/Sxlf4 females is sensitive to tetracycline.

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Acknowledgements

We thank L. Sefton for generating the original suppressed Sxlf4 strain, D. Presgraves for the y w CS Wolbachia strain, and B. J. Meyer for comments on the manuscript.

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Correspondence to Thomas W. Cline.

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Starr, D., Cline, T. A host–parasite interaction rescues Drosophila oogenesis defects. Nature 418, 76–79 (2002). https://doi.org/10.1038/nature00843

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