水稻细胞周期蛋白CYCP4调控低磷抑制生长的分子机制

Inorganic phosphate is one of the most essential and limiting nutrients in all organisms. Up to now, a number of genes have been reported to participate in regulation of phosphate deficiency responses in plant. However, few were discovered to regulate the growth inhibition of plant during phosphate starvation. In the budding yeast, Saccharomyces cerevisiae, PHO80-PHO85 complex is involved both in regulating the phosphate signal transduction (PHO) pathway and in controlling the G0 entry. Previously, we identified and cloned seven PHO80 homologous genes named OsCYCPs in rice. Among them, only the OsCYCP1;1 gene was able to partially rescue the pho80 mutant strain of yeast. OsCYCP1;1 influences the phosphate starvation signaling response, but does not affect the growth and the development of rice. Our previous work has demonstrated that CYCP4, a membrane of the CYCP gene family, is regulated by phosphate deficiency through transcriptional regulation. Preliminary results have also shown that CYCP4 negatively regulates plant growth and phosphate signaling. Hence, by analyzing the expression pattern of CYCP4 and studying both CYCP4 over-expressing and null plants, we aim to characterize the possible mechanism of CYCP4 in growth regulation during phosphate deficiency. Furthermore, by identifying it physical and genetic interacting partners, we want to eventually uncover the detailed molecular mechanism of CYCP4 in regulating plant growth and phosphate signaling during phosphate deficiency.

磷是一切生命所必需的大量元素之一。目前已报道参与磷饥饿信号调控网络的基因越来越多，但关于磷饥饿胁迫抑制植物生长的分子生理机制还很少。PHO80-PHO85复合体是酵母磷信号通路中重要负调控因子，同时还参与调控细胞周期中G0期的起始。OsCYCP是PHO80在水稻中的同源蛋白，我们发现其中OsCYCP1;1能部分回复pho80突变体磷信号，OsCYCP1;1能影响磷饥饿响应信号，但对植株的生长没有明显影响。前期的研究发现CYCP亚类成员CYCP4基因的表达受低磷诱导，初步结果表明CYCP4负调控水稻植株生长及磷信号。因此，本研究将通过系统分析CYCP4基因的表达模式，借助创制的过表达及功能缺失突变体解析其参与低磷信号及低磷胁迫下的植株生长的可能机制。同时，通过解析CYCP4的蛋白互作模式及其与磷信号关键调控因子的遗传关系，最终明确CYCP4参与低磷胁迫下水稻生长及磷信号途径的分子生理机制。

低磷胁迫抑制植株生长发育从而降低作物产量，但其作用的分子生理机制至今仍不清楚。为了研究这个问题，我们检测了低磷胁迫抑制水稻叶片生长的原因。结果表明，低磷胁迫主要通过抑制水稻地上部细胞分裂能力来抑制植株生长。PHO80-PHO85复合体是酵母磷信号通路中重要负调控因子，同时还参与调控细胞周期中G0期的起始。OsCYCP是PHO80在水稻中的同源蛋白，初步结果发现CYCP亚类成员CYCP4基因（不包括OsCYCP4;3）的表达受缺磷胁迫诱导受到长期，而增强表达这些低磷胁迫诱导的OsCYCP4能够抑制水稻生长。进一步研究发现，这些OsCYCP4蛋白通过与细胞周期蛋白竞争结合细胞周期蛋白依赖的激酶，从而影响细胞分裂速率。与这相一致，OsCYCP4的缺失突变体（cycp4;1, cycp4;2 和cycp4;4）与野生型相比，表现出对低磷胁迫抑制生长敏感度下降的表型。因此，我们的结果表明，低磷胁迫主要通过诱导OsCYCP4家族基因的表达，干扰细胞周期蛋白与细胞周期蛋白依赖的激酶互作，从而影响细胞分裂抑制水稻地上部生长，且这些低磷胁迫诱导OsCYCP4家族基因可以作为提高水稻耐低磷能力的潜在靶基因位点。