胚胎受热应激合成热休克蛋白（HSP）72，HSP72对胚胎耐热起重要的作用，然而胚胎如何调控HSP72表达目前尚不清楚。本项目拟以体外培养的小鼠胚胎为研究对象，通过热休克诱导胚胎HSP72表达、添加激动剂和抑制剂以及RNAi方法，采用荧光定量PCR、Western blot、免疫荧光组化和凝胶阻滞分析等技术，在筛选出CaM、CaMKⅡ和HSP72在胚胎中表达最佳条件的基础上，研究CaM-CaMKⅡ信号通路如何激活HSF1、HSF1三聚体磷酸化及其与DNA结合活性，进而影响HSP72表达，以阐明附植前小鼠胚胎HSP72表达信号转导的分子机制。研究成果将为深入研究热应激和热性疾病导致的哺乳动物妊娠早期胚胎死亡奠定理论基础。

The embryos synthetize heat shock protein (HSP)72 after being heat stressed and the HSP72 plays a crucial role in the embryos for resisting futher elevation of temperature. However, it is not clear, up to now, that how the embryos regulating this HSP72 expression. This project is planed to use preimplantation mice embryos as study subjects, and a number of methods will be employed in treating the experimental embryos, which include inducing HSP72 by heat shock, using agonists and inhibitors and RNA interfere. The techniques of qRT-PCR, Western blot, immunofluorescence histochemistry and electrophoreretic mobility shift assay etc. will be used in the experiments. On the basis of the optimum conditions selected for the expression of CaM, CaMKⅡ and HSP72 the embrionic HSP72 expression under heat shock condition regulating by CaM-CaMKⅡsignaling pathway including the activation of HSF1, the phosphorylation of HSF1 tripolyme and its binding activity to the HSE, which in turn influencing HSP72 expression,will be investigated in the objectives to reveal the mechanisms of signal transduction in the HSP72 expression of mice preimplantation embryos in the molecular level. The results will be useful for futher study the mechanism of embryo lose of the early pregnant mammalian in the hot summer or suffering from fervescence diseases.