Control of collective cell movement by planar cell polarity signaling

通过平面细胞极性信号控制集体细胞运动

• 批准号: 10403992
• 负责人: John B Wallingford
• 金额: $ 32.85万
• 依托单位: UNIVERSITY OF TEXAS AT AUSTIN
• 依托单位国家: 美国
• 财政年份: 2020
• 资助国家: 美国
• 起止时间: 2020-07-29 至 2025-05-31
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/10403992
• 关键词: Actins; Actomyosin; Adhesions; Animals; Award; Biological; Biological Process; C cadherin; Cadherins; Cell Adhesion; Cell Polarity; Cell-Cell Adhesion; Cells; Cellular biology; Congenital Abnormality; Cytoskeleton; Defect; Development; Developmental Biology; Etiology; Failure; Genetic; Goals; Human; Image; Integral Membrane Protein; Light; Limb structure; Link; Mediating; Morphogenesis; Movement; Neural Tube Closure; Neural Tube Defects; Organ; Pattern; Proteins; Proteomics; Resolution; Set protein; Signal Transduction; Speed; System; Time; Tissues; UPK3 gene; Vertebrates; Work; base; cell behavior; cell motility; cell type; cofilin; congenital anomaly; convergent extension; experimental study; genetic regulatory protein; in vivo; in vivo imaging; insight; planar cell polarity; protein protein interaction; skeletal dysplasia; success

Abstract Collective cell movements termed convergent extension (CE) drive the elongation of tissues and organs in essentially all animals. In vertebrates, CE is controlled by the planar cell polarity (PCP) signaling system, and defects in PCP-dependent convergent extension are associated with human neural tube defects and skeletal dysplasias. We feel that the profound lack of information regarding the basic cell biology of CE as it occurs in vertebrate animals in vivo represents the key challenge in the field at this time. Building on our recent successes in advanced imaging and proteomics, this proposal takes a "cell biological" approach, focusing on fundamental cellular machines of cadherin adhesion, actin assembly, and the septin cytoskeleton and how they are deployed to drive PCP-mediated CE.

抽象的 称为收敛扩展（CE）的集体细胞运动驱动组织和器官在 本质上是所有动物。在脊椎动物中，CE由平面细胞极性（PCP）信号系统控制，并且 PCP依赖性收敛扩展的缺陷与人类神经管缺陷和骨骼有关 发育不良。我们认为，关于CE的基本细胞生物学的严重缺乏信息 体内的脊椎动物代表了此时的主要挑战。建立在我们最近的 在高级成像和蛋白质组学中取得了成功，该建议采用了“细胞生物学”方法，重点是 钙粘蛋白粘附，肌动蛋白组装和隔蛋白细胞骨架的基本细胞机以及如何 它们被部署以驱动PCP介导的CE。