View Program - 63rd Annual Drosophila Research Conference

Mechanical input, much like a biochemical signal, can be converted into a biological response and trigger downstream effects. Adherens junctions, the major cell-cell junctions that resist physical tension, often mediate mechanosensitivity. Our lab has shown that in the mesoderm precursor epithelium of Drosophila gastrula, adherens junctions are strengthened in response to physical tension generated by apical myosin contraction. Such mechanosensitive junction strengthening is essential for mesoderm morphogenesis, but the molecular mechanism mediating this regulation is unknown. We have identified Gilgamesh (Gish) as a potential novel mechanosensitive junction regulator. Using multiple approaches, we show that Gish appears to be recruited to junctions in mesoderm upon Myosin activation but not in tissues without active Myosin. This recruitment is disrupted in alpha-catenin mutants, suggesting its dependency on adherens junctions. Importantly, loss of function of Gish leads to severe defects in adherens junctions and mesoderm internalization. Consistent with weakened adherens junctions, Gish mutants phenocopy junction mutants in membrane morphology. These data suggest Gish is a critical player in mechanosensitive remodeling of adherens junctions.

Characterization of mechanosensitive regulation of cell adhesion by membrane kinase Gish