Caloric density alters meiotic recombination rate in Drosophila melanogaster.

Plasticity in meiotic recombination is a well-documented phenomenon with an unknown mechanism. Recent studies have shown variation in the magnitude and direction of plasticity with a putative connection to organismal stress. Though there have been many factors shown to contribute to recombination rate plasticity, dietary manipulations are understudied. Here we manipulated caloric density, which is known to contribute to well-known life-history trade-offs, to determine if it altered meiotic recombination rates. To investigate the role of genetic background, we selected two stocks from the Drosophila Genetic Reference Panel (DGRP) with varying susceptibility to starvation stress. We found that overall recombination rates increased as calories decreased consistent with previous dietary plasticity studies in Drosophila. Specifically, while neither 0.5x nor 2x were significantly different from the standard 1x diet, we found significant post hoc differences between the low-calorie (0.5x) versus the high-calorie (2x) dietary treatments in the strain DGRP_42 but not in DGRP_217, confirming the predicted increased sensitivity of DGRP_42 to starvation stress based on prior studies. In addition to measuring changes in crossover frequency and distribution, we also investigated various organismal reproductive and physiological traits. We found significant changes in female body mass, the number of oocytes in female ovaries, and male testis length due to both diet and genetic background. We also noted significant differences in DNA damage during oogenesis via TUNEL assay. Examination of ovarian gene expression confirmed that the strain that had plasticity in recombination (DGRP_42) also had 20x more differentially expressed genes between dietary treatments. Despite diet typically eliciting a tradeoff whereby dietary restriction increases lifespan, here we saw evidence that DGRP_42 did not experience benefits from low-calorie treatment, with evidence of stress response and increased DNA damage, which suggests plasticity in recombination is due to stress. Overall, our study provides additional support for the negative relationship between metabolism and recombination rate, differences between genetic backgrounds, and a connection between organismal traits and plasticity in meiotic recombination.