植物茎尖分生组织（shoot apical meristem，SAM）是胚后发育地上部分所有器官的来源，器官发生开始于植物暗形态建成后被激活的干细胞产生的分生组织。在植物暗形态建成中植物下胚轴伸长，SAM及其干细胞活性被抑制。虽然暗中下胚轴伸长的机制得到大量研究，但是SAM被抑制的分子机制还不清楚。我们前期工作中筛选到一个拟南芥突变体asd1(activated SAM in darkness1)，暗中培养表现为正常的下胚轴伸长和激活的SAM。本项目将综合利用遗传学、细胞和分子生物学、生物化学及转录组学结合生物信息学，系统研究ASD1维持暗中分生组织活性的机制；ASD1介导光对激素信号调控作用的分子机制，最终解析ASD1调控暗-光形态建成中分生组织活性从休眠到激活的分子网络机制。

Plant shoot apical meristem (SAM) is critical for the ground-above postembryonic organogenesis that derives from the activated stem cells after skotomorphogenesis. During skotomorphogenesis, plants produce elongated hypocotyl and a hook that protects the repressed SAM. While numerous studies were focused on the hypocotyl elongation in darkness, the mechanisms underlying how the SAM is repressed are mainly unclear. Previously, we isolated one Arabidopsis mutant that displays normal hypocotyl elongation but activated SAM in darkness. In this project, with genetic analysis, molecular and cellular analysis, biochemistry assay as well as RNA-seq combined with bioinformatics analysis, we will focus on the molecular mechanisms of ASD1 in SAM maintenance and activation, the roles of ASD1 in light-regulated phytohormones on the SAM activation. Eventually, we will dissect the regulatory network in ASD1-mediated SAM maintenance and activation during the phase change from skotomorphogenesis to photomorphogenesis.