Signaling to Cell Intercalation in Arabidopsis

这个项目的长期目标是了解细胞嵌入的潜在信号机制， 在这种情况下，相邻的细胞会改变它们的形状，成为彼此的夹层。细胞嵌入是 对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 原肠形成、神经分化、轴伸长过程中收敛伸展所必需的 动物和人类胚胎的器官发生。然而，支配这一基本原理的信号和途径 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)在动植物王国中被认为是保守的。在模式植物拟南芥中， 细胞嵌入对叶表皮的发育很重要，叶表皮细胞在叶表皮中发育。 中间的裂片和凹痕形成拼图外观。PI的团队已经开发出 路面细胞作为细胞嵌入的模型系统，建立了RHO的第一个框架 控制这一过程的依赖GTP酶的细胞内信号网络。它由两个部分组成 拮抗通路：激活叶形成的ROP2-RIC4-肌动蛋白通路和ROP6-RIC1- 促进压痕形成的微管途径。在这个项目中，信号、受体和新的组件将 确定并与这一框架相联系。在目标1中，激活ROP2 GTP酶的信号事件，例如， SPK1ROP鸟嘌呤核苷酸交换因子的信号转导将用生化， 遗传学和细胞生物学方法。在目标2中，将确定ROP6 GTP酶上游的分子 使用类似的方法，ROP6和ROP2通路之间的细胞间信号将是 调查以了解相邻细胞之间如何协调裂片和缩进。目标3 是研究生长素梯度是如何作为发育信号诱导中间生长的。一个 将使用rop突变和生化和细胞生物学检测相结合的方法来确定 生长素激活ROP2或ROP6途径。插入所需的TMK受体样激酶 生长将测试它们对生长素感知的参与程度。从这些目标出发，全面了解 我们将揭示牙间生长的分子和细胞机制。 考虑到植物和人类之间细胞嵌入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提供新的见解 分机。因为汇聚延伸失败会导致神经管缺陷(NTDS)，这是一种常见的 发育障碍(1000例妊娠中有1例)，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. ^_^^