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Enrique Rodríguez

Publications and source records attributed to Enrique Rodríguez.

2 recordsLinked to original sources
PubMed2026

Mitochondrial genetic effects mediate the response to stress through development, but not adult metabolic rate in Drosophila.

Energy expenditure is fundamental to physiology, behaviour, ecology, and life history, yet the mechanisms that regulate metabolic rate remain poorly understood. At the cellular level, incompatibilities between the maternally inherited mitochondrial genome and the nuclear genome can impair energy production, signalling and gene expression, with potential to disrupt a wide range of physiological processes. However, how these often-subtle genomic mismatches influence whole-organism traits such as metabolic rate, activity, and fitness remains unclear. Here, we generated mitonuclear-mismatched fly lines to test how early-life dietary and metabolic stress affect larval and adult physiology. Our results revealed sex and line-specific physiological effects, with larval development, survival and female fertility strongly contingent on the haplotypes and treatment, while adult resting metabolic rate and activity were not influenced by mitochondrial haplotype, nor by developmental stress.

Drosophila melanogaster↗
PubMed2025

The metabolic costs of meiotic drive.

Selfish genetic elements, such as meiotic drive genes, disrupt Mendel's law of equal segregation by biasing their own transmission, often at a detriment to the rest of the genome. Metabolic costs of the X-linked sex ratio (SR) meiotic drive were investigated in stalk-eyed flies (Teleopsis dalmanni). The experiments demonstrate that individuals with SR have reduced capacity for ATP synthesis. The disruption in mitochondrial function leads to compensation exhibited in increased basal metabolic rate and greater food consumption across a range of diets. The range of metabolic costs of drive was evident in males and females at a similar magnitude. The likely cause lies in the accumulation of deleterious mutations within the series of large inversions on the drive X chromosome, subject to low recombination and weak natural selection. In females, the drive chromosome had a dominant effect, with a single copy causing substantial metabolic compromise. There was little evidence of male-specific metabolic costs, nor evidence of greater effects of drive chromosomes on female metabolism. This suggests that direct metabolic costs from meiotic drive on spermatogenesis and from sexually antagonistic selection are relatively weak. Our results underscore the broad physiological impacts that selfish genetic elements have on host metabolism and fitness.

Animals↗