Signaling to Cell Intercalation in Arabidopsis

该项目的长期目标是了解细胞嵌入的潜在信号机制， 其中相邻的细胞改变它们的形状以彼此插入。细胞嵌入是 对于多细胞生物体的正常发育和形态发生至关重要。细胞嵌入是 在原肠胚形成、神经胚形成、轴伸长过程中， 动物和人类胚胎的器官形成。然而，控制这一基础的信号和途径 过程的特征很差，尽管一些潜在的信号事件（例如，Rho GTP酶和 细胞骨架）已知在动物和植物界中是保守的。在模式植物拟南芥中， 细胞嵌入对于叶表皮的发育是重要的，其中铺面细胞发育 中间的裂片和凹痕形成拼图的外观。Pi的团队开发了 路面细胞作为模型系统的细胞嵌入，并建立了第一个框架的Rho 控制这一过程的依赖GTP酶的细胞内信号网络。它由两个 抵消途径：ROP 2-RIC 4-肌动蛋白途径激活叶形成和ROP 6-RIC 1-肌动蛋白途径激活叶形成。 微管途径促进压痕。在这个项目中，信号，受体和新的组件将被 与这个框架相联系。在目的1中，激活ROP 2 GT3的信号传导事件，例如， 通过SPK 1 ROP鸟嘌呤核苷酸交换因子的信号传导，将使用生物化学， 遗传学和细胞生物学方法。在目标2中，将确定ROP 6 GTdR上游的分子 使用类似的方法，ROP 6和ROP 2通路之间的细胞间信号传导将被 研究以了解如何在相邻细胞之间协调成瓣和缩进。目标3 是研究生长素梯度，作为一个发展的信号，诱导插入生长。一 ROP突变体与生物化学和细胞生物学测定的组合将用于确定 生长素激活ROP 2或ROP 6途径。TMK受体样激酶是细胞间质调节所必需的。 将测试它们参与生长素感知的生长。从这些目标出发， 揭示了插层生长的分子和细胞机制。 考虑到植物和人类细胞嵌入背后的信号机制的保守性， 从这项研究中获得的知识可能会为我们理解收敛性提供新的见解。 扩展名.由于会聚延伸的失败会导致神经管缺陷（NTD）， 发育障碍（1/1000怀孕），这项研究与人类健康有关 改进. ^_^^

The long-term goal of this project is to understand the underlying signaling mechanisms of cell intercalation, in which neighboring cells change their shapes to become intercalated with each other. Cell intercalation is critical for the proper development and morphogenesis of multi-cellular organisms. Cell intercalation is required for the process of convergent extension during gastrulation, neurulation, axis elongation, and organogenesis of animal and human embryos. However, signals and pathways governing this fundamental process are poorly characterized, though some underlying signaling events (e.g., Rho GTPases and the cytoskeleton) are known to be conserved across animal and plant kingdoms. In the model plant Arabidopsis, cell intercalation is important for the development of the leaf epidermis, in which pavement cells develop intercalary lobes and indentations to form the jigsaw-puzzle appearance. The Pi's group has developed the pavement cell as a model system for cell intercalation, and has established the first framework of a Rho GTPase-dependent intracellualr signaling network that controls this process. It is composed of two counteracting pathways: a ROP2-RIC4-actin pathway activating lobe formation and a ROP6-RIC1- microtubule pathway promoting indentation. In this project, signals, receptors and new components will be determined and linked to this framework. In aim 1, signaling events activating the ROP2 GTPase, e.g., signaling by the SPK1 ROP guanine nucleotide exchange factor, will be investigated using biochemical, genetic, and cell biological methods. In aim 2, molecules upstream of the ROP6 GTPase will be determined using similar approaches, and the intercellular signaling between the ROP6 and the ROP2 pathways will be investigated to understand how lobing and indenting are coordinated between the neighboring cells. Aim 3 is to investigate how auxin gradients, acting as a developmental signal, induce intercalary growth. A combination of rop mutants and biochemical and cell biological assays will be used to determine whether auxin activates the ROP2 or ROP6 pathway. The TMK receptor-like kinases that are required for intercalary growth will be tested for their participation in auxin perception. From these aims, a comprehensive picture of the molecular and cellular mechanisms for intercalary growth will be revealed. Given the conservation of the signaling mechanisms underlying cell intercalation across plants and humans, the knowledge gained from this research may provide new insights into our understanding of convergent extension. Because failure in convergent extension causes neural tube defects (NTDs), a common developmental disorder (1 out of 1000 pregnancies), this research is relevant to human health improvements. ^_^^