<i>Drosophila</i> female fertility and juvenile hormone metabolism depends on the type of <i>Wolbachia</i> infection

Abstract

Maternally inherited intracellular bacteria <i>Wolbachia</i> cause both parasitic and mutualistic effects on their numerous insect hosts, including manipulating the host reproductive system in order to increase the bacteria spreading in a host population, and increasing the host fitness. Here, we demonstrate that the type of <i>Wolbachia</i> infection determines the effect on <i>Drosophila melanogaster</i> egg production as a proxy for fecundity, and metabolism of juvenile hormone (JH), which acts as gonadotropin in adult insects. For this study, we used six <i>D. melanogaster</i> lineages carrying the nuclear background of interbred Bi90 lineage and cytoplasmic backgrounds with or without <i>Wolbachia</i> of different genotype variants. The <i>w</i>MelCS genotype of <i>Wolbachia</i> decreases egg production in infected <i>D. melanogaster</i> females in the beginning of oviposition and increases it later (from the sixth day after eclosion), whereas the <i>w</i>MelPop <i>Wolbachia</i> strain causes the opposite effect, and the <i>w</i>Mel, <i>w</i>Mel2 and <i>w</i>Mel4 genotypes of <i>Wolbachia</i> do not show any effect on these traits compared with uninfected Bi90 <i>D. melanogaster</i> females. The intensity of JH catabolism negatively correlates with the fecundity level in the flies carrying both <i>w</i>MelCS and <i>w</i>MelPop <i>Wolbachia</i> The JH catabolism in females infected with genotypes of the <i>w</i>Mel group does not differ from that in uninfected females. The effects of <i>w</i>MelCS and <i>w</i>MelPop infection on egg production can be levelled by the modulation of JH titre (via precocene/JH treatment of the flies). Thus, at least one of the mechanisms promoting the effect of <i>Wolbachia</i> on <i>D. melanogaster</i> female fecundity is mediated by JH.