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

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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.