氨氮是水产养殖中诱发疾病爆发的重要环境因子。细胞凋亡在机体应对各种环境胁迫时发挥重要的作用。我们前期研究发现，氨氮胁迫能导致青蟹血细胞凋亡率升高，并且与ATM、p53基因表达上调具有密切的关系，但其调控机制尚不清楚。本项目以青蟹为研究对象，采用流式细胞等方法对氨氮胁迫诱导青蟹血细胞凋亡特征以及凋亡相关因子进行检测，确定细胞凋亡的发生；采用荧光定量PCR和Western Blot等技术分析ATM/p53信号通路与细胞凋亡的相关性。同时采用RNA干扰和转录组学等技术，研究ATM/p53信号通路激活或抑制对细胞凋亡的影响，并解析该信号通路调控细胞凋亡的分子网络路径。本研究结果不仅对深入了解甲壳动物防御的分子机理具有重要的理论意义，而且对青蟹健康养殖和疾病防控具有重要的实际意义。

Ammonia is an important environmental factor which can induce disease outbreak in aquaculture. Apoptosis plays a crucial role in many biological processes, including development, cellular homeostasis and immune responses. Previous study suggested that ammonia stress could induce apoptosis in mud crab. Moreover, the mRNA levels of ATM and p53 significantly up-regulated under ammonia stress. However, the molecular mechanism remains unclear. In this study, we investigate the effects of ammonia stress on apoptosis. We study the correlation between ATM/p53 signaling pathways and apoptosis using quantitative real-time PCR and western blot. The effects of activated or inactivated ATM/p53 signaling pathways on apoptosis under ammonia stress will be studied via RNAi. Meanwhile, we identified the molecular network pathway of ATM/p53 on regulating apoptosis in response to ammonia stress. This study will provide a new theory about the molecular mechanisms of the crustacean defense, and will also provide a new way for the development of high effective strategy for disease control of mud crab.