海参极强的自溶能力给其贮藏、保鲜和加工带来诸多难题。研究发现，海参自溶时钙网蛋白表达上调，且出现细胞凋亡特征。钙网蛋白过表达可触发内质网应激及相关凋亡。 然而，对于内质网应激是否引起海参自溶，钙网蛋白作为应激关键分子如何介导凋亡等问题，目前仍未明确。 本项目拟从凋亡信号传导的角度研究海参自溶现象。首先，在紫外诱导海参自溶和内质网应激诱导剂作用的海参细胞模型上，采用细胞损伤检测、RT-PCR和/或Western blotting检测确定内质网应激相关凋亡引起海参自溶；其次，采用特异性干扰剂调节钙网蛋白上调或抑制表达，确定海参自溶时钙网蛋白是引起内质网应激相关凋亡的关键分子；最后， 在钙网蛋白干预表达的紫外诱导海参自溶细胞模型上， 进一步探明钙网蛋白介导内质网应激相关凋亡引起海参自溶的信号途径。 从而，为揭示海参自溶机理奠定理论基础。

Sea cucumber with the strong ability of autolysis introduces a serious problems with respect to its storage, preservation and processing. Previously results have showed that, carlreticulin (CRT) upregulated during sea cucumber autolysis and accompanied by apoptosis. And over-expression of CRT could trigger endoplasmic reticulum stress (ERS)-related apoptosis. However, the issues are not clear that whether ERS-related sea cucumber apoptosis triggered sea cucumber autolysis, and how the signaling pathway of CRT, as the key factor, induces ERS-related apoptosis. This project intends to figure out the signaling pathway of apoptosis during sea cucumber autolysis. Firstly, based on the models of UV-induced sea cucumber autolysis and tunicamycin (TM)-induced ERS, cell apoptosis and necrosis will be assessed. ER specific resident fluorochrome Dapoxyl will be used to observe ER morphological changes. RT-PCR and/or Western blotting will be used to detect expression of ERS molecules and apoptosis-related molecules. It will suggest that ERS induces sea cucumber apoptosis and then triggers sea cucumber autolysis. Secondly, in order to investigate whether CRT is the key factor to induce ERS-related apoptosis during sea cucumber autolysis, specific interference agents will be used to interfere with CRT expression. Finally, the signaling pathway of CRT-mediated ERS apoptosis during sea cucumber autolysis will be investigated basing on the model of UV-induced sea cucumber autolysis with over-expression of CRT. Thus, the results of this research would lay the theoretical foundation for revealing the mechanism of sea cucumber autolysis.