Biology subjects

Yoshinari, Y.

Publications and source records attributed to Yoshinari, Y..

4 recordsLinked to original sources

bioRxiv2025

Microbiome-host interactions drive a trade-off between sleep quality and lifespan in Drosophila

Understanding the interactions between various aging processes and the resulting heterogeneity in aging is crucial for promoting healthy aging. Here, we provide evidence that heterogeneity in microbiome and host interactions contributes to diversifying aging phenotypes in sleep, gut integrity, and longevity in Drosophila. Aged flies exhibiting sleep fragmentation preserve gut integrity, accompanied by a shift in microbiota composition, particularly an increase in Acinetobacter junii. A. junii induces sleep fragmentation via its metabolite, urocanic acid, through serotonin receptor-dependent dopamine upregulation. In parallel, A. junii exploits the host response to promote its growth, leading to lifespan extension, which is recapitulated by genetically modified Escherichia coli, suggesting a trade-off between sleep quality and lifespan. Our study demonstrates a systematic mechanism underlying aging heterogeneity, suggesting interventions through bacterial supplements.

animal behavior and cognition↗

bioRxiv2025

Genome-wide association study shows developmental robustness control by intestinal maltase via internal environment in Drosophila

Organisms encounter disturbances during development because of genetic variations, environmental shifts, and stochastic noise. However, developmental robustness and canalization buffer these fluctuations to maintain normal development. Nevertheless, understanding the underlying mechanisms that govern this robustness is challenging because of the complex interactions between these factors. In Drosophila, the number of scutellar sensory organs (SSO; macrochaetes) derived from the sensory organ precursors (SOPs) in the larval wing disc has been used as a model to study developmental robustness. Although the number of SOPs is strictly regulated by a network of signaling and transcription factors in the imaginal disc, non-intrinsic broader factors such as temperature and energy metabolism additionally influence SSO-number fluctuation. Moreover, the precise molecular mechanisms regulating the systemic control of bristle number remain unknown. In this study, we identify factors controlling bristle robustness by performing genome-wide association studies (GWAS). We observed significant single-nucleotide polymorphisms (SNPs) in the Maltase gene cluster and found that the knockdown of Maltase genes affected SSO numbers. Furthermore, Maltase-A1(Mal-A1) in the gut regulated insulin signaling systemically, thereby affecting SSO-number fluctuation. These results suggest that Mal-A1 contributes to robustness by modulating glucose availability and Drosophila insulin-like peptide 3 (dilp3) level, which affects the SOPs in a nonautonomous manner. This study presents the molecular basis of nutritional regulation of developmental robustness and highlights Maltase as a key mediator.

developmental biology↗

bioRxiv2021

The sugar-responsive enteroendocrine neuropeptide F regulates lipid metabolism through glucagon-like and insulin-like hormones in Drosophila melanogaster

The enteroendocrine cell (EEC)-derived incretins play a pivotal role in regulating the secretion of glucagon and insulins in mammals. Although glucagon-like and insulin-like hormones have been found across animal phyla, incretin-like EEC-derived hormones have not yet been characterised in invertebrates. Here, we show that the midgut-derived hormone, Neuropeptide F (NPF), acts as the sugar-responsive, incretin-like hormone in the fruit fly, Drosophila melanogaster. Secreted NPF is received by NPF receptor in the corpora cardiaca and in insulin-producing cells. NPF-NPFR signalling resulted in the suppression of the glucagon-like hormone production and the enhancement of the insulin-like peptide secretion, eventually promoting lipid anabolism. Similar to the loss of incretin function in mammals, loss of midgut NPF led to significant metabolic dysfunction, accompanied by lipodystrophy, hyperphagia, and hypoglycaemia. These results suggest that enteroendocrine hormones regulate sugar-dependent metabolism through glucagon-like and insulin-like hormones not only in mammals but also in insects.

physiology↗

bioRxiv2020

Neuronal octopamine signaling regulates mating-induced germline stem cell proliferation in female Drosophila melanogaster

Stem cells fuel the development and maintenance of tissues. Many studies have addressed how local signals from neighboring niche cells regulate stem cell identity and their proliferative potential. However, the regulation of stem cells by tissue-extrinsic signals in response to external cues remains poorly understood. Here we report that efferent octopaminergic neurons projecting to the ovary are essential for germline stem cell (GSC) proliferation in response to mating in female Drosophila. The neuronal activity of the octopaminergic neurons is required for mating-induced GSC proliferation as they relay the mating signal from Sex peptide receptor-positive cholinergic neurons. Octopamine and its receptor Oamb are also required for mating-induced GSC proliferation via intracellular Ca2+ signaling. Moreover, we identified Matrix metalloproteinase-2 as a downstream component of the octopamine-Ca2+ signaling to induce GSC proliferation. Our study provides a mechanism describing how neuronal system couples stem cell behavior to external cues through stem cell niche signaling.

developmental biology↗