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Melo-Gavin, C.

Publications and source records attributed to Melo-Gavin, C..

4 recordsLinked to original sources

Local Adaptation to the Sex Environment: Reciprocal Sex-Limited Selection in Different Thermal Regimes

The shared genome prevents each sex from independently responding to the selection experienced by that sex. We used experimental evolution in Drosophila melanogaster with separate pools of Chromosome 3s for males (male-limited chromosomes) and females (female-limited chromosomes) for 15 generations. Viewing each sex as a separate environment, we performed a reciprocal transplant between the sexes to quantify the strength of local adaptation to each sex environment. Each chromosome type was more beneficial in the sex it had been selected for (i.e., local adaptation to sex). Because it has been postulated that sex differences in selection may depend on how well adapted a population is to the abiotic environment, we performed experimental evolution at two thermal regimes: one benign temperature to which the populations were well-adapted and one novel temperature. Female-specific adaptation was stronger at the benign temperature whereas male-specific adaptation was stronger in the novel temperature. Within chromosome pools, male and female fitness were more positively correlated in the novel compared to the benign temperature. Though males carrying male-limited chromosomes were typically more fit than males carrying female-limited chromosomes, they were also more harmful to their female mating partners.

evolutionary biology↗

Response of mate harm to sex-separated gene pools

Competition among males to fertilize females can generate sex differences in selection. At the genetic level, alternative alleles can be favoured in each sex (intralocus sexual conflict, IASC). At the phenotypic level, males can evolve traits that are harmful to the females with whom they interact. Here we used experimental evolution in Drosophila melanogaster to examine how relaxing IASC affected the evolution of mate harm. Genetically variable Chromosome 2s evolved in two separate pools within each population. One pool experienced patrilinear inheritance (segregated like a Y-chromosome) and male-limited selection, while the alternative pool segregated like an X-chromosome and experienced female-biased selection. We measured female fitness when exposed to males carrying either chromosome type at either normal (continuous) or reduced (periodic) male exposure, over three time periods. Males carrying either type of chromosome were harmful to females, but males carrying a male-limited chromosome displayed increased harmfulness, suggesting ongoing selection for mate harm that is constrained under normal inheritance. The magnitude and direction of the effect of male interaction on female fitness was highly sensitive to time of measurement, and we observed a brief period where increased interaction with males was beneficial to females.

evolutionary biology↗

Genomic response to sex-separated gene pools

Males and females experience differences in the strength and direction of selection but discerning the type of genes that are targets of sex differences in selection is complicated by their shared genome. We used experimental evolution in Drosophila melanogaster to partially separate the gene pools of males and females for 130 generations. In six replicate populations, we forced one pool of genetically variable Chromosome 2s to experience patrilinear inheritance (segregating like a Y-chromosome) and male-limited selection. The alternative pool segregated like an X-chromosome and experienced female-biased selection. This allowed alleles which are differentially selected for between the sexes to diverge between these pools, enabling us to gain insight into the type of genes subject to such selection. We find that genes which diverge between these pools have an elevated intersexual genetic correlation(rMF) for expression on average, consistent with the idea that high genetic correlations may hinder sex-specific adaptation under normal inheritance. Diverged genes were also enriched for moderately male-biased genes whereas female-biased genes were underrepresented. At the SNP level, we find an overrepresentation of diverged SNPs involved in splicing or occurring in the 5UTR and an underrepresentation of missense or synonymous SNPs, suggesting sex differences in selection for isoform usage.

evolutionary biology↗

Large cells activate global protein degradation to maintain cell size homeostasis

Proliferating animal cells maintain a stable size distribution over generations despite fluctuations in cell growth and division size. This tight control of cell size involves both cell size checkpoints, which delay cell cycle progression in small cells, and size-dependent regulation of mass accumulation rates. While we previously identified the p38 MAPK pathway as a key regulator of the mammalian cell size checkpoint, the mechanism of size-dependent growth rate regulation has remained elusive. Here, we quantified global rates of protein synthesis and degradation in cells of varying sizes, both under unperturbed conditions and in response to perturbations that trigger size-dependent compensatory growth slowdown. We found that protein synthesis rates scale proportionally with cell size across cell cycle stages and experimental conditions. In contrast, oversized cells that undergo compensatory growth slowdown exhibit a superlinear increase in proteasome-mediated protein degradation, with accelerated protein turnover per unit mass, suggesting activation of the proteasomal degradation pathway. Both nascent and long-lived proteins contribute to the elevated protein degradation during compensatory growth slowdown, with long-lived proteins playing a crucial role at the G1/S transition. Notably, large G1/S cells exhibit particularly high efficiency in protein degradation, surpassing that of similarly sized or larger cells in S and G2, coinciding with the timing of the most stringent size control in animal cells. These results collectively suggest that oversized cells reduce their growth efficiency by activating global proteasome-mediated protein degradation to promote cell size homeostasis.

cell biology↗