我所前期空间飞行实验发现水稻在空间分蘖和叶夹角比地面大，与重力相关的OsLAZY1的表达量明显下调，而拟南芥中LAZY基因过表达使侧枝夹角明显变小。LAZY1是一个参与早期重力刺激信号转导的蛋白，但参与过程的分子机制仍然不清楚。通过同源比对分析我们发现LAZY1的N端保守序列与已报导的N端降解子序列非常相似。本课题从蛋白质翻译后修饰角度研究拟南芥LAZY1的积累与降解参与重力刺激信号转导的分子机制。通过质谱鉴定到LAZY1的泛素化修饰位点和磷酸化位点，对这些位点进行了点突变，拟通过表型观察和蛋白水平确认泛素化降解系统参与LAZY1重力刺激信号转导机制，并验证LAZY的泛系化过程是依赖于其自身的磷酸化修饰。通过IP-MS和转录组鉴定能够使LAZY1磷酸化和泛素化的激酶和E3泛素连接酶，并通过突变体表型与Co-IP实验来验证。结合LAZY1的上下游通路提出LAZY1转导重力刺激信号的机制。

In our previous space experiment, we have found that the tiller and leaf angles of the rice were larger in space and the expression of OsLAZY1 was decreased significantly than those grown on the ground. However, overexpression of the Arabidopsis LAZYs can result in the narrow branch angle, which is quite opposite from the phenotype of decreased expression of LAZY1. As we known, LAZY1 is one of the gravity related genes particularly participated in the early stage of gravity sensing but the implied mechanism involved in the sensing process is still obscure. By homologous alignment analysis, we found that the conserved N-terminal sequence of LAZY1 was very similar to the reported N-degron. In our study, we conducted the experiment from the view of protein post translation modification (PTM) to investigate the accumulation and degradation of LAZY1 involving in the gravity sensing mechanism. Mass spectrometry based PTM experiments enable the identification of the ubiquitination and phosphorylation sites of the LAZY1 protein and the corresponding sites mutation transgenetic Arabidopsis seedlings are accessible to analyze the function of LAZY1 involving in the gravity sensing from both the phenotype and the protein level. Furthermore, the dependence of the phosphorylation of LAZY1 ubiquitination in our model needs to be further elucidated. Transcriptomics and IP-MS analysis will be applied in our investigation to further explore the regulators of LAZY1 especially the E3 ligase and the kinase which can specifically recognize LAZY1 as the substrate under the stimulus of gravity. Both the Co-IP and phenotype observation will be applied to validate the implied candidates of interactors. In conclusion, we propose potential mechanism regulating LAZY1 mediated gravity sensing and signal transduction.