Molecular mechanisms patterning viscosity of the junctional network during Drosophila pupal wing morphogenesis

果蝇蛹翅形态发生过程中连接网络粘度的分子机制

• 批准号: 273684262
• 负责人: Professor Dr. Stephan Wolfgang Grill, since 7/2020
• 金额: --
• 依托单位: Max-Planck-Institut für molekulare Zellbiologie und Genetik (MPI-CBG)
• 依托单位国家: 德国
• 项目类别: Priority Programmes
• 财政年份: 2015
• 资助国家: 德国
• 起止时间: 2014-12-31 至 2022-12-31
• 项目状态: 已结题
• 来源: https://gepris.dfg.de/gepris/projekt/273684262?language=en
• 关键词: Molecular; mechanisms; patterning; viscosity; junctional

Reshaping of the Drosophila pupal wing is a viscous deformation that occurs in response to anisotropic tissue stress. To understand stress-induced shape changes in development, we must understand the spatiotemporal dynamics of tissue stresses, and the regional patterns of tissue viscoelasticity that specify how tissue deforms under stress. The viscoelastic properties of wing tissue arise both from the viscoelastic properties of its constituent cells, and from its ability to undergo stress-dependent cell rearrangements. We showed previously that cell elongation in the wing epithelium depend on stress-dependent changes in the endocytic turnover of E-Cadherin, and that Core Planar Cell Polarity (PCP) proteins and p120 Catenin are essential components of a mechanism that tunes E-Cadherin turnover in response to stress. Here, we propose to elucidate how tissue stresses in the wing influence the localization and dynamics of key components of the E-Cadherin adhesion machinery and the cytoskeleton, and how p120 and PCP proteins influence these responses. We will examine whether PCP proteins act as stress sensors, and examine their influence on the polarity of adhesive protein dynamics. Finally, we will investigate spatial patterns of tissue viscoelasticity and study the molecular basis of these differences. These experiments will lead us to a multiscale understanding of how the shape of the wing emerges from patterned tissue mechanical properties.

果蝇蛹翅膀的重塑是在各向异性组织应力作用下发生的粘性变形。为了了解应力在发育过程中引起的形状变化，我们必须了解组织应力的时空动态，以及组织粘弹性的区域模式，这些模式指定了组织在压力下如何变形。翅膀组织的粘弹性特性既来自其组成细胞的粘弹性特性，也源于其经历应力依赖的细胞重排的能力。我们以前已经证明，翅膀上皮细胞的伸长依赖于E-钙粘附素内吞周转的应激变化，而核心平面细胞极性(PCP)蛋白和p120连环蛋白是调节E-粘附素周转以响应应激的机制的重要组成部分。在这里，我们建议阐明翅膀上的组织应力如何影响E-钙粘附素黏附机制和细胞骨架的关键部件的定位和动力学，以及p120和PCP蛋白如何影响这些反应。我们将研究PCP蛋白是否作为应力传感器，并检测它们对黏附蛋白动力学的极性的影响。最后，我们将研究组织粘弹性的空间模式，并研究这些差异的分子基础。这些实验将引导我们多尺度地理解翅膀的形状是如何从有图案的组织机械特性中出现的。