cAMP-epac-rap1信号通路在热激诱导家蚕非减数分裂孤雌生殖发生中的作用和机制研究

细胞学研究显示家蚕非减数分裂孤雌生殖的发生是减数分裂第一次成熟分裂中期的纺锤体被破坏，从而使同源染色体早期分离，形成未减数的原核。热激信号通过哪些信号通路调控纺锤体形成受阻是阐明热激诱导家蚕非减数分裂孤雌生殖发生的关键。我们前期通过转录组比较分析筛选到cAMP-Epac-Rap1通路在热激诱导后的孤雌生殖系中特异激活，已有研究表明该信号通路能调控减数分裂纺锤体形成过程。本研究拟通过信号分子的表达变化验证，定量磷酸化蛋白质组筛选信号通路关键分子的活化位点，明确cAMP-Epac-Rap1的响应，通过信号通路的抑制和活化验证其在孤雌生殖热激诱导中的作用，并进一步筛选信号通路关键因子Rac1的下游作用因子，分析相互间的调控关系，本研究能初步揭示cAMP-Epac-Rap1信号通路在家蚕非减数分裂孤雌生殖发生中的作用机制，为解析家蚕孤雌生殖发生分子机制提供新的理论知识。

Cytological studies have shown that the ameiotic parthenogenesis of silkworm is attribute to the destruction of the spindle in the first stage of meiosis, which causes the homologous chromosomes to be separated early and form unreduced pronuclei. It is critical to clarify the heat shock-induced ameiotic parthenogenesis of silkworm by which the heat shock signal regulates the formation of spindle. We have previously screened the cAMP-Epac-Rap1 pathway for specific activation in parthenogenetic lines following heat shock induction by transcriptome comparison analysis. Studies have shown that this signaling pathway can regulate the process of meiotic spindle formation. This study is to detect the expression of the key molecules and their activation sites by phosphorylation proteome, and then verify the response of cAMP-Epac-Rap1 in parthenogenetic heat stimulation. The down signal factors of Rac1 will be further screened, and their regulation relationship be studied. This study can preliminary reveal the role of cAMP-Epac-Rap1 signaling pathway in ameiotic parthenogenesis in silkworm. The results will provide important information for the study of the molecular mechanism of parthenogenesis in silkworm.