Inhibin βB Mediates Oligotrophic Adaptation via Regulating Muscle Satellite Cell Proliferation and Differentiation in Schizopygopsis younghusbandi

Adaptive reprogramming to oligotrophic environments is a key evolutionary strategy for extreme-habitat species. While enhanced fat storage and autophagy activation are well-elucidated, the molecular basis of growth retardation remains undefined. The Qinghai-Tibet Plateau shows decreasing nutrient availability with rising elevation, and its endemic Schizopygopsis younghusbandi is an ideal model for nutrient scarcity adaptation. We mimicked nutrient deficiency via in vitro low-serum and in vivo starvation assays, identifying that inhibin βB acts centrally: its upregulation activates the SMAD pathway, inducing G1 phase arrest, attenuated proliferation, and reduced energy consumption. Nutrient deprivation also upregulates pdgf-c to induce a fibrotic phenotype in muscle satellite cells. In vivo assays verified inhibin βB elevation, reversible upon refeeding. We established a S. younghusbandi muscle satellite cell culture system, elucidating inhibin βB-mediated adaptive mechanisms. Comparative sequence analysis across eight Cyprinid species revealed high conservation (>90%) of inhibin βB, suggesting evolutionary preservation. These findings uncover molecular underpinnings of high-altitude schizothoracine adaptive evolution to nutrient scarcity, and broaden insights into survival strategies of organisms in extreme oligotrophic habitats.