1. ¹Center for Insect Science, University of Arizona, Tucson, AZ, USA
2. ²Department of Entomology, University of Arizona, Tucson, AZ, USA
3. ³Department of Biology, University of Victoria, Victoria, British Columbia, Canada

Correspondence: Dr JA White, Department of Entomology, University of Kentucky, S-225 Agricultural Science Center North, Lexington, KY 40546, USA. E-mail: jenwhite.uk@gmail.com

Received 6 August 2008; Revised 22 November 2008; Accepted 23 December 2008; Published online 18 February 2009.

Abstract

Many bacterial endosymbionts of insects are capable of manipulating their host's reproduction for their own benefit. The most common strategy of manipulation is cytoplasmic incompatibility (CI), in which embryonic mortality results from matings between uninfected females and infected males. In contrast, embryos develop normally in infected females, whether or not their mate is infected, and infected progeny are produced. In this way, the proportion of infected females increases in the insect population, thereby promoting the spread of the maternally inherited bacteria. However, what happens when multiple endosymbionts inhabit the same host? The parasitoid wasp Encarsia inaron is naturally infected with two unrelated endosymbionts, Cardinium and Wolbachia, both of which have been documented to cause CI in other insects. Doubly infected wasps show the CI phenotype. We differentially cured E. inaron of each endosymbiont, and crossed hosts of different infection status to determine whether either or both bacteria caused the observed CI phenotype in this parasitoid, and whether the two symbionts interacted within their common host. We found that Wolbachia caused CI in E. inaron, but Cardinium did not. We did not find evidence that Cardinium was able to modify or rescue Wolbachia-induced CI, nor did we find that Cardinium caused progeny sex ratio distortion, leaving the role of Cardinium in E. inaron a mystery.