1A–C) is the higher levels of vg, vgR and hex 70a transcripts in non-infected

bees fed beebread compared to the infected bees fed the same diet. These results indicate that infection significantly prevented up-regulation of vg, vgR and hex 70a genes in the bees fed beebread. Infection also prevented the increase in the levels of vg and hex 70a transcripts (but not of vgR transcripts) in syrup-fed bees, although this effect was much less obvious than that shown by beebread-fed bees ( Fig. 1A–C). Bees fed on royal jelly showed low and similar levels of vg, vgR and hex 70a transcripts, regardless of infection ( Fig. 1A–C). In contrast to vg, vgR and hex 70a, neither the diet nor the infection altered the expression of the apoLp-III ( Fig. 1D) and apoLp-II/I genes ( Fig. 1E). Similar to apoLp-II/I, the expression of apoLpR did not change as a HSP inhibitor consequence of the infection ( Fig. 1F), however, the apoLpR gene was the only to show a higher expression in the bees fed syrup

in comparison to those fed beebread. To validate the above findings, we investigated the abundance of vg, hex 70a, and apoLp-II/I gene products in hemolymph of the bees fed the different diets and infected. The Vg, Hex 70a, and ApoLp-I (the major subunit derived from the post-translational cleavage of ApoLp-II/I) proteins are secreted by the fat body into the hemolymph, where they accumulate in large quantities. Similar to the transcription levels, we observed the highest Vg and Hex 70a levels in the hemolymph of the non-infected beebread-fed Alpelisib supplier bees. Intermediate and low, or very low, levels were respectively found in the other non-infected groups, fed royal jelly or syrup ( Fig. 2). Infection impaired the normal accumulation of Vg and Hex 70a in Farnesyltransferase the hemolymph of the bees fed beebread or royal jelly and this was more evident for Vg than for Hex 70a. Infection did not show any obvious effect on the hemolymph level of either protein in the bees fed syrup ( Fig. 2). Comparisons

of the ApoLp-I levels among the non-infected groups suggest that ApoLp-I accumulation is diet-dependent. However, this analysis was somewhat hindered due to the inconsistent levels of ApoLp-I in the hemolymph of bees fed on each of the protein-rich diets. In any case, the infection only slightly impaired the storage of ApoLp-I, independent of the diet supplied ( Fig. 2). All the bee groups showed similar survival rates, regardless of diet or infection (Supplementary file 1). To ensure that the bees were feeding normally, we also measured the volume of food consumed daily. There was no significant difference among the groups of bees (Supplementary file 2). We explored the relationships between diet (nutrition), ovary activation and response to infection in the honey bees. Because the worker bees used in this study were maintained without a queen, some of them were able to activate their ovaries.