Abstract

Turbot ( Scophthalmus maximus ) is a commercially important farmed fish, but normal reproductive development consumes substantial energy, reducing growth and survival. By producing sterile triploid fish, which possess three sets of chromosomes, this energy is redirected toward growth, conferring significant benefits for aquaculture. However, the molecular mechanisms underlying triploid sterility remain poorly understood. In this study, we examined ovarian development in diploid (normal) and triploid (sterile) turbot at three key stages (6, 10, and 20 months after hatching). Histological analysis revealed that triploid ovaries failed to develop normally, with eggs unable to mature. By analyzing gene activity, we identified widespread disruptions in processes essential for egg formation, energy production, and cell survival, ultimately causing ovarian underdevelopment. Notably, we observed a shift from early elimination of defective germ cells to later maintenance of cellular stability. These findings explain why triploid turbot are sterile and provide a valuable foundation for improving triploid production efficiency in aquaculture, supporting more sustainable fish farming practices. Triploid turbot ( Scophthalmus maximus ) exhibit superior growth and survival, yet the molecular basis of their sterility—a key trait for aquaculture—remains largely unexplored. This study investigated ovarian development and transcriptomic profiles in diploid and triploid S. maximus at three key stages (6, 10, and 20 months post-hatch, mph) to elucidate the stage-specific molecular mechanisms underlying triploid sterility. Histological analysis revealed that diploid ovaries progressed through normal oogenesis to the early vitellogenic stage by 20 mph, whereas triploid ovaries were arrested at the oogonial stage, with only occasional primary oocytes and extensive connective tissue infiltration. Comparative transcriptomic analysis identified 13,305, 14,599, and 13,331 differentially ex