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

果蝇蛹翅的重塑是一种粘性变形，是对各向异性组织应力的响应。为了理解应力诱导的发育过程中的形状变化，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应力下如何变形。翅膀组织的粘弹性特性源于其组成细胞的粘弹性特性，以及其进行应力依赖性细胞重排的能力。我们之前的研究表明，翅膀上皮细胞的伸长取决于E-Cadherin的内噬转换的应力依赖性变化，并且核心平面细胞极性（PCP）蛋白和p120 Catenin是调节E-Cadherin在应激反应中转换机制的重要组成部分。在这里，我们建议阐明翅膀中的组织应力如何影响e -钙粘蛋白粘附机制和细胞骨架的关键成分的定位和动力学，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，并研究它们对粘附蛋白动力学极性的影响。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。这些实验将使我们对翅膀的形状如何从图案组织力学特性中产生有多尺度的理解。

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.