Biology subjects

Nogueira Alves, A.

Publications and source records attributed to Nogueira Alves, A..

5 recordsLinked to original sources

bioRxiv2026

Dietary landscapes shape genotype- and sex-specific responses to insecticides

Insecticide resistance is typically studied as a response to chemical toxicity, yet in natural and agricultural systems insecticides are embedded within food resources. How resistance alleles interact with nutritional environments to shape fitness remains largely unknown. Here we combine nutritional geometry approaches to test how variation at a major resistance locus, Cyp6g1, modifies sex-specific reproductive performance across dietary landscapes in Drosophila melanogaster. We show that a resistance allele does more than increase survival: it profoundly reshapes reproductive allocation in both sexes. Resistant females exhibited up to a two-fold increase in ovariole number, with benefits amplified in protein-rich, high-calorie diets. In contrast, resistant males displayed increased testis size but reduced seminal vesicle and accessory gland size, revealing sex-specific trade-offs. Critically, contaminating doses of imidacloprid shifted nutritional optima according to genotype, in some cases enhancing reproduction in susceptible flies, consistent with diet-dependent hormesis. Thus, resistance, nutrient availability and toxin exposure jointly determine fitness outcomes. Our findings demonstrate that resistance evolution is embedded within dietary landscapes rather than driven by toxicity alone, highlighting the need to integrate nutritional ecology into predictions of resistance dynamics in human-modified environments.

ecology↗

bioRxiv2025

Dissecting contributions of directional and balancing selection to trajectories of mitochondrial haplotype evolution in Drosophila melanogaster.

Emerging evidence suggests mtDNA haplotypes contribute to fitness variation and local adaptation, with studies highlighting the potential for directional selection, imposed by distinct thermal environments, and negative frequency-dependent selection to shape spatial patterns of mtDNA haplotype diversity. However, the interplay between these different forms of selection remains unexplored. To address this, we conducted experimental evolution using Drosophila melanogaster populations derived from opposite ends of a latitudinal cline in Australia (Melbourne and Townsville), exposing them to contrasting thermal environments and varying starting frequencies of two mtDNA haplotypes (A1 and B1) that each segregate at high frequencies in natural populations. We paired this approach with population genetic simulations to estimate selection and its influence on haplotype evolutionary trajectories. We found that mtDNA haplotype frequencies were influenced by complex interactions among temperature, starting frequency, and nuclear genomic background (Melbourne, Townsville, or admixed). Simulations supported directional selection as a driver of haplotype frequencies in populations evolving at 17{degrees}C in the Melbourne background, and otherwise selection was predominantly balancing and shaped by negative frequency-dependent fitness effects of the haplotypes. Finally, our results suggest that the thermal environment is not the sole environmental variable shaping mitochondrial evolutionary dynamics and point to a possible role for mito-nuclear epistasis.

evolutionary biology↗

bioRxiv2024

Mammalian heat shock protein A4 family ortholog Hsc70Cb is required for two phases of spermatogenesis in D. melanogaster

Heat shock proteins play essential roles as molecular chaperones, enacting protein folding and preventing of protein aggregation. In a previous study, a predicted damaging homozygous non-synonymous genetic variant was detected in the heat shock protein gene HSPA4L. Here, we used RNA interference in Drosophila melanogaster to explore the role of the heat shock protein A member 4 family (HSPA4) family in male fertility. Expression of the fly orthologue of the mammalian HSPA4 and HSPA4L genes, Hsc70Cb, was ablated in the male germline using two RNAi lines and the Nanos-Gal4 driver. Strong knockdown of Hsc70Cb in male germ cells resulted in male sterility, characterised by the absence of germ cells in testes and the over-proliferation of the testis soma. A less robust knockdown of Hsc70Cb in the male germline resulted in a sperm individualisation defect and a failure of sperm release into the seminal vesicle (analogous to the epididymis). When human HSPA4 or HSPA4L cDNA was introduced into infertile Hsc70Cb mutant flies, a partial rescue was observed, whereby in the robust Hsc70Cb knockdown setting germ cells progressed to the spermatocyte stage before undergoing cell death. Collectively, the absence of sperm in the Hsc70Cb (line 1) is consistent with the infertile man harbouring a homozygous HSPA4L genetic variant, supporting the hypothesis that HSPA4L is required for male fertility in humans and flies and highlighting the utility of the fly as a model of human spermatogenesis. In briefHsc70Cb is essential for spermatogonia survival and sperm individualisation in Drosophila. This study highlights the conserved roles of the HSPA4 family across animals and the utility of flies as a model organism for male fertility research.

genetics↗

bioRxiv2021

Target of Rapamycin drives unequal responses to essential amino acid depletion in egg laying

Nutrition shapes a broad range of life history traits, ultimately impacting animal fitness. A key fitness-related trait, female fecundity is well known to change as a function of diet. In particular, the availability of dietary protein is one of the main drivers of egg production, and in the absence of essential amino acids egg laying declines. However, it is unclear whether all essential amino acids have the same impact on phenotypes like fecundity. Using a holidic diet, we fed adult female D. melanogaster diets that contain all necessary nutrients except one of the 10 essential amino acids and assessed the effects on egg production. For most essential amino acids, depleting a single amino acid induced as rapid a decline in egg production as when there were no amino acids in the diet. However, when either methionine or histidine were excluded from the diet, egg production declined more slowly. Next, we tested whether GCN2 and TOR were involved in this difference in response across amino acids. While mutations in GCN2 did not eliminate the differences in the rates of decline in egg laying among amino acid drop-out diets, we found that inhibiting TOR signalling caused egg laying to decline rapidly for all drop-out diets. TOR signalling does this by regulating the yolk-forming stages of egg chamber development. Our results suggest that amino acids differ in their ability to induce signalling via the TOR pathway. This is important because if phenotypes differ in sensitivity to individual amino acids, this generates the potential for mismatches between the output of a pathway and the animals true nutritional status.

developmental biology↗

bioRxiv2020

Ecdysone coordinates plastic growth with robust pattern in the developing wing

Animals develop in unpredictable, variable environments. In response to environmental change some aspects of development adjust to generate plastic phenotypes. Other aspects of development, however, are buffered against environmental change to produce robust phenotypes. How organ development is coordinated to accommodate both plastic and robust developmental responses is poorly understood. Here, we demonstrate that the steroid hormone ecdysone coordinates both plasticity of organ size and robustness of organ pattern in the developing wings of the fruit fly Drosophila melanogaster. Using fed and starved larvae that lack prothoracic glands, which synthesise ecdysone, we show that nutrition regulates growth both via ecdysone and via an ecdysone-independent mechanism, while nutrition regulates patterning only via ecdysone. We then demonstrate that growth shows a graded response to ecdysone concentration, while patterning shows a threshold response. Collectively, these data support a model where nutritionally-regulated ecdysone fluctuations confer plasticity by regulating disc growth in response to basal ecdysone levels, and confers robustness by initiating patterning only once ecdysone peaks exceeds a threshold concentration. This could represent a generalizable mechanism through which hormones coordinate plastic growth with robust patterning in the face of environmental change.

developmental biology↗