C型钠肽（CNP）通过受体（NPR2）调节cGMP合成，是近年来重点研究的卵母细胞减数分裂核心控制通路。LH峰之后，CNP-NPR2-cGMP通路快速失活是减数分裂恢复的标志性事件。虽然此前文献报道了LH引发下游NPR2去磷酸化失活和cGMP主动降解的机制，但都不能合理解释减数分裂的恢复。因此，阐明整个信号最上游源头配体CNP及其编码基因Nppc mRNA快速下降的机制，就显得十分必要。我们的前期工作发现，LH可诱导卵泡中具有mRNA降解活性的锌指蛋白TTP快速表达，并靶向Nppc mRNA 3’UTR，使其迅速降解。在此基础上，课题将以小鼠和牛为模型，从CNP-NPR2-cGMP通路上游入手，研究TTP降解Nppc mRNA在减数分裂恢复中的作用，以及LH诱导TTP的调控路径和作用方式，这不仅有助于回答减数分裂恢复启动的关键机制，也将为预防和解决家畜及人类卵母细胞成熟失败的难题提供参考。

The cGMP production controlled by C-natriuretic peptide (CNP) and its receptor (NPR2), is the critical pathway responsible for oocyte meiosis. After LH surge, inactivation of CNP-NPR2-cGMP pathway is the hallmark of meiotic resumption. Previous studies have reported that LH-induced dephosphorylation and inactivation of NPR2, as well as cGMP hydrolysis may be implicated in this process, however, the critical mechanisms underlying the inactivation of CNP-NPR2-cGMP pathway, has never been determined. Thus, it is of prime importance to unveil the detailed mechanism responsible for the rapid decrease of upstream ligand CNP and is coding gene Nppc. Our pilot study showed that LH induced a specific zinc finger protein Tristetraprolin (TTP) that can facilitate rapid mRNA degradation. Further study indicated that TTP binds to 3’UTR of Nppc mRNA, and led to its rapid degradation. In the present study, using mouse and bovine as models, we aim to determine the role of TTP-induced Nppc mRNA degradation, in oocyte meiotic resumption, as well as the pathway underlying LH-induced TTP. These finding, will be helpful for understanding the key mechanism of oocyte meiotic resumption, and provide a reference for preventing the oocyte maturation failure in both animals and humans.