早期胚胎发生中胚柄细胞程序性死亡的初始信号及其转导途径

During early embryogenesis suspensor cells play a critical role in embryo development.as the embryo develops the suspensor cells timely undergo programmed cell death and finally disappears. The molecular mechanism regulating this essential developmental process still remains largely unknown today. Our previous work revealed that NtCYS-NtCP14 is a bipartite molecular module to switch on the suspensor PCD, and thus provides a unique opportunity to seek more detailed regulatory machinery. In this project we try to screen the primary signal and its transduction pathway for the initiation of PCD in suspensor cell. This project may provide unique knowledge on embryogenesis in relation to maternal tissue and suspensor and valuable reference for understanding molecular mechanism of PCD during plant development.

被子植物早期胚胎发生过程中胚柄细胞对于胚胎发育具有至关重要的作用。当胚胎发育至一定阶段，胚柄细胞总是适时启动细胞程序性死亡（PCD）过程并最终自行降解消失。对于这一重要发育过程的了解已近百年，但对其分子调控机制迄今仍所知甚少。我们的前期工作发现NtCYS-NtCP14作为一个双分子开关调控胚柄细胞PCD的启动，从而为探讨PCD分子调控机制提供了难得的切入点。在本项目中我们拟进一步解析NtCYS-NtCP14上游的调控机制，寻找调控胚柄细胞程序性死亡的初始信号及其传导途径，力求较为完整的认识启动胚柄细胞PCD的机理。这一工作不仅可对阐述胚柄发育与胚体和母体组织的关系提供独特的证据，对认识植物其它器官中细胞程序性死亡的作用和调控机制也有普遍意义。

我们的前期工作发现NtCYS-NtCP14作为一个双分子开关调控胚柄细胞PCD的启动，为探讨PCD分子调控机制提供了难得的切入点。在本项目中我们进一步解析了NtCYS-NtCP14上游的调控机制，明确了调控胚柄细胞程序性死亡的初始信号GA4及其传导途径。发现GA4可适时地瞬时升高，并由珠孔端母体细胞进入胚柄，触发DELLA降解，解除其对CYS转录的激活作用，使得CYS表达停止，释放了NP14的活力，启动胚柄PCD。这一工作揭示了GA的作用机制及与胚柄PCD的直接联系。这一工作较为完整的揭示了启动胚柄细胞PCD的机理，对阐述胚柄发育与胚体和母体组织的关系提供了明确的证据，也有助于认识植物其它器官中细胞程序性死亡的作用和调控机制。