Abstract：
Sea cucumber is a valuable seafood product and autolysis is the main concern for the aquaculture industry. This study employed proteomics and transcriptomics to investigate the autolysis mechanism of sea cucumbers. The fresh sea cucumber was exposed to UV light to induce autolysis. The body wall samples were cut off to analyze by proteomics and transcriptomics. The angiotensin-converting enzyme (ACE) inhibitor of teprotide and the activator of imatinib were gastric gavage to live sea cucumbers, respectively, to identify the regulation target. Autolysis occurrence was evaluated by appearance, soluble peptide, and hydroxyproline content. Four gene-protein pairs were ACE, AJAP10923, Heme-binding protein 2-like, and Ficolin-2-like. Only the ACE protein and gene changed synchronously and a significant down-regulation of ACE occurred in the autolysis sea cucumbers. Teprotide led to a 1.58-fold increase in the TCA-soluble protein content and a 1.57-fold increase in hydroxyproline content. No significant differences were observed between imatinib-treated sea cucumbers and fresh ones regarding TCA-soluble protein content or hydroxyproline levels (P > 0.05). ACE inhibitor accelerated the autolysis of sea cucumber, but ACE activator inhibited the autolysis. Therefore, ACE can serve as a regulatory target for autolysis in sea cucumbers.
摘要：
海参是一种有价值的海鲜产品，自溶是水产养殖业的主要关注点。本研究采用蛋白质组学和转录组学研究海参的自溶机制。将新鲜海参暴露于UV光以诱导自溶。切除体壁样品以通过蛋白质组学和转录组学进行分析。teprotide的血管紧张素转换酶（ACE）抑制剂和伊马替尼的激活剂对活海参进行了胃灌胃，分别,确定调控目标。通过外观评估自溶的发生，可溶性肽，和羟脯氨酸含量。四种基因-蛋白质对是ACE，AJAP10923,血红素结合蛋白2-like,和Ficolin-2-like.在自溶海参中，只有ACE蛋白和基因同步变化，并且ACE发生了显着下调。Teprotide导致TCA可溶性蛋白质含量增加1.58倍，羟脯氨酸含量增加1.57倍。伊马替尼处理的海参与新鲜海参之间在TCA可溶性蛋白含量或羟脯氨酸水平方面没有观察到显着差异（P>0.05）。ACE抑制剂加速海参自溶,但ACE激活剂抑制自溶。因此,ACE可以作为海参自溶的调控目标。
