Is lipid synthesis plasticity in Leptopilina heterotoma due to methylation as epigenetic marks ?
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- Parasitoids are holometabolous insects whose adult form is a free-living insect with a parasitic larval stage, which grows and feeds using the body of a single arthropod host. It was first believed that it was impossible for parasitoid wasps to accumulate fat for storage, and scientists wanted to investigate if the loss of lipid synthesis was correlated with parasitism in insects. Visser et al (2010) investigated this question and concluded that the evolution of a lack of lipid synthesis was concurrent with the evolution of parasitism in insects and had been facilitated by environmental compensation. However, they also found that some species re-evolved lipid synthesis. After this, Visser et al collected Leptopilina heterotoma populations in Europe and Asia. These populations showed, on the one hand, variability in lipid synthesis, and on the other hand, a genetic homogeneity. They thus suggested that these results could be explained by plasticity in lipid synthesis. In order to investigate this hypothesis, Visser et al (2019) performed GC-MS on wasps coming from a split-brood family design experiment in which mothers were allowed to lay eggs either on lean D. simulans or fat D. melanogaster, thus revealing a higher lipid synthesis in the low-fat environment (D.sim) than in the high-fat environment (D.mel), definitely proving that there is plasticity for lipid synthesis and that this plasticity is due to environmental conditions. The current hypothesis is that methylation, as epigenetic marks, is a mechanism that underlies lipid synthesis plasticity, where environmental cues of fat quantity are integrated during larval development inside the host, leading to modification of epigenetic patterns, and thus resulting in a phenotype that is able to switch lipid synthesis on or off through modified DNA transcription. Moreover, as DNA methylation decreases DNA availability, resulting in a reduced transcription of the genes on which methylation takes place, we expect the genes governing lipid metabolism to be more methylated/heavily methylated in a high-fat environmental context, thus turning off lipid synthesis. Thus, a similar split-brood design experiment will be performed, with three major differences. First, the offspring will be cut in half, as one half will undergo GC-MS and assess the ability or not to synthesize lipids, while the other half will be used to assess the methylation patterns. Second, the mothers will be submitted to three environments, rich, medium and poor in fat that have been investigated and carefully chosen. Third, inbred lines will be used, in order to decrease genetic heterogeneity and ease statistical processes. However, the timings have been such that the split-brood design experiment is carried out at the same time as this work is written, and its results therefore cannot be discussed here.