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Goldner, A. N.

Publications and source records attributed to Goldner, A. N..

2 recordsLinked to original sources

Tissue recoil in the early Drosophila embryo is a passive not active process

Understanding tissue morphogenesis is impossible without knowing the mechanical properties of the tissue being shaped. Although techniques for measuring tissue material properties are continually being developed, methods for determining how individual proteins contribute to mechanical properties are very limited. Here, we developed two complementary techniques for the acute inactivation of sqh (the Drosophila myosin regulatory light chain), one based on the recently introduced AID2 system, and the other based on a novel method for conditional protein aggregation. Combining these techniques with rheological measurements, we show that passive material properties of the cellularization-stage Drosophila embryo are essentially unaffected by myosin activity. The significance of this study is two-fold. We introduce a system for the nearly instantaneous inactivation of proteins in a variety of systems. Additionally, we demonstrate a method to distinguish between active and passive contributions to effective tissue elasticity. SummaryTechniques to examine the contribution of specific proteins to tissue mechanical properties are extremely limited. Here, Goldner et al. develop two complementary techniques for rapid protein depletion combined with mechanical measurements, and show that myosin activity is dispensable for tissue elasticity.

cell biology↗

What basal membranes can tell us about viscous forces in Drosophila ventral furrow formation

Ventral furrow (VF) formation in Drosophila melanogaster is an important model of epithelial folding. Previous models of VF formation require cell volume conservation to convert apically localized constriction forces into lateral cell elongation and tissue folding. Here, we investigated embryonic morphogenesis in anillin knockdown (scra RNAi) embryos, where basal cell membranes fail to form and therefore cells can lose cytoplasmic volume through their basal side. Surprisingly, the mesoderm elongation and subsequent folding that comprise VF formation occurred essentially normally. We hypothesized that the effects of viscous shear may be sufficient to drive membrane elongation, providing effective volume conservation, and thus driving tissue folding. Since this hypothesis may not be possible to test experimentally, we turned to a computational approach. A minimal model of VF formation accounting for fluid dynamics indicated that shear forces can indeed explain our experimental observation. However, this conclusion depended on specific values of the model parameters. To test whether viscous shear is a dominant force for morphogenesis in vivo, we developed a highly realistic computational model incorporating both accurate cell and tissue geometry and experimentally measured material parameters. Results from this model demonstrate that viscous shear generates sufficient force to drive cell elongation and tissue folding in vivo.

developmental biology↗