Abstract
Contractile actomyosin networks have been shown to power tissue morphogenesis. Although the basic cellular machinery generating mechanical tension appears largely conserved, tensions propagate in unique ways within each tissue. Here we use the vertebrate eye as a paradigm to investigate how tensions are generated and transmitted during the folding of a neuroepithelial layer. We record membrane pulsatile behavior and actomyosin dynamics during zebrafish optic cup morphogenesis by live imaging. We show that retinal neuroblasts undergo fast oscillations and that myosin condensation correlates with episodic contractions that progressively reduce basal feet area. Interference with lamc1 function impairs basal contractility and optic cup folding. Mapping of tensile forces by laser cutting uncover a developmental window in which local ablations trigger the displacement of the entire tissue. Our work shows that optic cup morphogenesis is driven by a constriction mechanism and indicates that supra-cellular transmission of mechanical tension depends on ECM attachment.
Highlights
The shape of animal organs evolved by natural selection under constrains imposed both by organ physiology in the adult and tissue mechanics during embryogenesis
Contractile forces are transmitted to neighboring cells and to the extracellular matrix (ECM) through cadherin and integrin receptors, allowing individual cell contributions to be integrated into tensions at the tissue/organ level (Papusheva and Heisenberg, 2010; Lecuit et al, 2011)
To formally show that basal constriction is taking place as the optic cup forms, we investigated the behavior of retinal precursors by live-imaging analysis
Summary
The shape of animal organs evolved by natural selection under constrains imposed both by organ physiology in the adult and tissue mechanics during embryogenesis. The main force generator during morphogenesis results from the molecular interaction between myosin II motors and the actin filaments at the cellular cortex (Salbreux et al, 2012). This actomyosin contractile apparatus sustains cortical tension, pulling cells into shape during development and tissue homeostasis. Regardless the morphogenetic context, actomyosin contractile forces are resisted both by cellular adhesions and by the compression of the internal cytoskeleton itself This results in a balance of forces that stabilizes transiently cell and tissue shapes for each stage of the developmental program that builds up a given organ
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