female fertility and juvenile hormone metabolism depends on the type of infection.

Maternally inherited intracellular bacteria 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 infection determines the effect on 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 lineages carrying the nuclear background of interbred Bi90 lineage and cytoplasmic backgrounds with or without of different genotype variants. The MelCS genotype of decreases egg production in infected females in the beginning of oviposition and increases it later (from the sixth day after eclosion), whereas the MelPop strain causes the opposite effect, and the Mel, Mel2 and Mel4 genotypes of do not show any effect on these traits compared with uninfected Bi90 females. The intensity of JH catabolism negatively correlates with the fecundity level in the flies carrying both MelCS and MelPop The JH catabolism in females infected with genotypes of the Mel group does not differ from that in uninfected females. The effects of MelCS and 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 on female fecundity is mediated by JH.