This study investigated the adaptive mechanisms of silver pomfret in response to chronic low-temperature stress, focusing on the tissue-specific expression patterns of the key lipid metabolism gene scd1 and its central role in regulating hepatic apoptosis. A gradual cooling experiment (from 18 °C to 6 °C) was conducted to analyze the spatiotemporal expression profiles of ten lipid metabolism-related genes across six tissues. The results revealed that the most pronounced changes were observed in the heart, liver, and gills. The liver and heart rapidly activated genes involved in lipid breakdown and utilization from 16 to 12 °C for immediate energy supply, while gill tissue upregulated the pi3k/p450/srebp/scd1 pathway at 10 °C to remodel membrane lipids against sustained stress. Further in vitro hepatocyte experiments demonstrated that scd1 expression directly regulated cell survival and apoptosis under low temperatures. Knockdown of scd1 significantly promoted apoptosis, whereas its overexpression effectively suppressed it. Moreover, scd1 expression was intricately modulated by its upstream regulators srebp (positive regulation) and pparγ (showing potential negative feedback at specific temperatures). This study systematically elucidates the pivotal role of scd1-mediated lipid metabolic reprogramming in the cold adaptation of silver pomfret, providing a crucial theoretical foundation for deciphering the molecular mechanisms of cold tolerance and for breeding cold-resistant strains.
Zhang et al. (Tue,) studied this question.