谷子CDL1（Curvy and Droopy Leaf 1）调控株型的分子机制研究

Foxtail millet, originated from China, is an important minor cereal, and currently being developed as the model for functional study in Panicoideae subfamily. Leaf architecture is one of the important components of plant architecture, and largely influences grain yield. Previously, we map-based cloned a novel player involving in regulation of leaf or plant architecture using a curvy and droopy leaf (cdl) mutant in foxtail millet. CDL1 encodes a leucine-rich repeat receptor-like kinase, and represses Brassinosteroids (BR) signaling to modulate leaf or plant architecture. However, the molecular mechanism underlying the negative regulation of BR signaling is still largely unknown. Moreover, the defective phenotypes of cdl1 dynamically change with the plant development showing curvy leaf at initial seedling stage, which is fully rescued at jointing stage, and gradually develops into droopy leaf after heading. This dynamic change appears to tightly associate with CDL1’s age-dependent tissue expression. Here, we will uncover the molecular mechanisms of BR signal regulation by CDL1 during leaf or plant architecture determination through a variety of protein interaction technologies, and explore what and how the endogenous cues control CDL1’s spatio-temporal expression. The results of this project will add the novel component and molecular mechanisms for BR signaling, and further extend the knowledge of the regulation of plant architecture by BR signaling.

谷子起源于我国，是重要的杂食作物，现逐步成为黍亚科的模式植物。叶片的形态建成是构成株型的重要因素，对禾谷类粮食作物的产量具有重要影响。我们在前期利用一个卷/披垂叶谷子突变体cdl1，图位克隆了一个新的参与植物叶/株型调控的膜蛋白类受体激酶基因。初步研究表明CDL1通过负调控油菜素内酯（Brassinosteroids, BR）信号来控制谷子的叶/株型，然而其调控BR信号的分子机制还不清。cdl1在苗期表现为卷叶，拔节期恢复至野生型，抽穗后叶片显著披垂，这种动态突变叶型与CDL1年龄依赖的组织时空性表达紧密相关。本项目将结合多种蛋白质互作技术解析CDL1在株型决定中调控BR信号的分子机制；研究植物利用何种内源信号控制CDL1组织时空性表达。从而将增添新的植物BR信号转导原件及分子机制，拓展人们对BR信号调控株/叶型的认识。

作物的叶片形态建成直接影响冠层结构，因此可影响产量。叶片的披垂度可影响叶片形态建成，是禾谷类作物的重要农艺性状。然而调控叶片披垂度的遗传学基础及分子机制仍然不清楚。在本项目中，我们图位克隆了谷子的一个LRR型膜蛋白受体激酶DPY1（为了避免与拟南芥中基因混淆，将CDL1重新命名为DPY1），其通过调节油菜素内脂（BR）信号的输出来调节谷子叶片的披垂度。组织特异性表达分析表明DPY1偏好性地在叶片维管组织中表达；DPY1的缺失会导致维管束的异常及叶片中木质素含量的降低，从而导致叶片本身支撑度不够而披垂。在分子机制上，DPY1与BR共受体BAK1互作，从而竞争性地抑制BR受体复合体BRI1/BAK1的形成、BRI1的磷酸化及下游BR信号的激活，DPY1抑制BR信号和叶片披垂度要依赖其激酶活性。此外，外源施加BR能够增强DPY1蛋白的积累及与BAK1的互作的亲和力，因此DPY1以一种“刹车”机制防止BR信号的过度激活。超表达玉米DPY1的同源基因能够完全恢复dpy1叶片披垂的表型，证实其功能在禾谷类作物中的保守性。最后，我们发现超表达DPY1的部分株系表现为紧凑直立叶型、更粗壮的茎秆及更大穗子，暗示其在谷子株型改良中的潜力。因此本项目揭示了BR信号如何被DPY1监视来确保叶片直立性的分子机制。

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