Meeting Abstract
To connect genes to processes that drive morphogenesis requires analysis of the impact of specific genes on the varied structures that contribute to mechanical properties of the embryo. Gastrulation and axis elongation in vertebrate embryos involves remodeling a sphere or disk of cells into a long body plan that resembles that of the adult. By contrast with later morphogenetic movements that shape complex 3D structures, axis extension proceeds as a relatively simple rearrangement of cells in a 2D plane. Using the elongating dorsal tissues of the Xenopus embryo, our group has developed a complete set of experimental tools and theory for direct biomechanical analysis to study tissue self-assembly. In this presentation I apply a M.A.R.K.-style biomechanical analysis to investigate structural origins of changing tissue mechanical properties through manipulations on the large-scale laminar structure of the embryo, control of cell size, and cell cortical cytoskeleton. Embryonic tissues increase stiffness nearly 10-fold over the course of gastrulation. Surprisingly, we find little contribution from emerging large scale structures in the embryo, such as the central column-like notochord or lateral beam-like pre-somitic mesoderm. However, the major contributor to changing tissue mechanical properties appears to lie in the cytoskeletal composition, but not thickness of the cell cortex. Expression of mutant and full length forms of the F-actin cross-linker protein α-actinin (ACTN1) alter tissue mechanics to the same magnitude as observed during development. Further analyses of modulators of the actomyosin cell cortex will uncover how gene regulatory networks establish and control embryonic as well as somatic tissue mechanical properties.
