Genetics, Vol. 155, 167-178, May 2000, Copyright © 2000

Offsetting Effects of Wolbachia Infection and Heat Shock on Sperm Production in Drosophila simulans: Analyses of Fecundity, Fertility and Accessory Gland Proteins

Rhonda R. Snooka, Sophia Y. Clelandb, Mariana F. Wolfnerb, and Timothy L. Karra
a Department of Organismal Biology and Anatomy, The University of Chicago, Chicago, Illinois 60637
b Department of Molecular Biology and Genetics, Cornell University, Ithaca, New York 14853

Corresponding author: Timothy L. Karr, Department of Organismal Biology and Anatomy, 1027 E. 57th St., The University of Chicago, Chicago, IL 60637., tkarr{at}midway.uchicago.edu (E-mail)

Communicating editor: A. G. CLARK

Infection in Drosophila simulans with the endocellular symbiont Wolbachia pipientis results in egg lethality caused by failure to properly initiate diploid development (cytoplasmic incompatibility, CI). The relationship between Wolbachia infection and reproductive factors influencing male fitness has not been well examined. Here we compare infected and uninfected strains of D. simulans for (1) sperm production, (2) male fertility, and (3) the transfer and processing of two accessory gland proteins, Acp26Aa or Acp36De. Infected males produced significantly fewer sperm cysts than uninfected males over the first 10 days of adult life, and infected males, under varied mating conditions, had lower fertility compared to uninfected males. This fertility effect was due to neither differences between infected and uninfected males in the transfer and subsequent processing of accessory gland proteins by females nor to the presence of Wolbachia in mature sperm. We found that heat shock, which is known to decrease CI expression, increases sperm production to a greater extent in infected compared to uninfected males, suggesting a possible link between sperm production and heat shock. Given these results, the roles Wolbachia and heat shock play in mediating male gamete production may be important parameters for understanding the dynamics of infection in natural populations.





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