Abstract

Spiroplasma poulsonii is a vertically transmitted endosymbiont of Drosophila melanogaster that causes male‐killing, that is the death of infected male embryos during embryogenesis. Here, we report a natural variant of S. poulsonii that is efficiently vertically transmitted yet does not selectively kill males, but kills rather a subset of all embryos regardless of their sex, a phenotype we call ‘blind‐killing’. We show that the natural plasmid of S. poulsonii has an altered structure: Spaid, the gene coding for the male‐killing toxin, is deleted in the blind‐killing strain, confirming its function as a male‐killing factor. Then we further investigate several hypotheses that could explain the sex‐independent toxicity of this new strain on host embryos. As the second non‐male‐killing variant isolated from a male‐killing original population, this new strain raises questions on how male‐killing is maintained or lost in fly populations. As a natural knock‐out of Spaid, which is unachievable yet by genetic engineering approaches, this variant also represents a valuable tool for further investigations on the male‐killing mechanism.

Highlights

  • Insects frequently harbour symbiotic bacterial population within their tissues (Buchner, 1965; Kikuchi, 2009)

  • We show that the mutant has a clean deletion of Spaid, presenting a unique opportunity to study the equivalent of a Spaid full knock-out, which is technically not achievable yet by genetic engineering

  • A natural variant of S. poulsonii exhibiting weak male killing has been identified and the low MK phenotype was tied to a lower endosymbiont titre in the adult females

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Summary

Introduction

Insects frequently harbour symbiotic bacterial population within their tissues (Buchner, 1965; Kikuchi, 2009). This strain causes an alternate phenotype in Drosophila whereby some infected offspring is killed regardless of the sex of the embryo.

Results
Conclusion

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