Search bioRxiv⌕ Search

bioRxiv · 10.1101/2023.08.14.553194

Cyclic muscle contractions reinforce the acto-myosin motors and mediate the full elongation of C. elegans embryo

Abstract

The paramount importance of mechanical forces in morphogenesis and embryogenesis is widely recognized, but understanding the mechanism at the cellular and molecular level remains challenging. Because of its simple internal organization, Caenorhabditis elegans is a rewarding system of study. As demonstrated experimentally, after an initial period of steady elongation driven by the actomyosin network, muscle contractions operate a quasi-periodic sequence of bending, rotation and torsion, that leads to the final 4-fold size of the embryo before hatching. How actomyosin and muscles contribute to embryonic elongation is investigated here theoretically. A filamentary elastic model that converts stimuli generated by biochemical signals in the tissue into driving forces, explains embryonic deformation under actin bundles and muscle activity, and dictates mechanisms of late elongation based on the effects of energy conversion and dissipation. We quantify this dynamic transformation by stretches applied to a cylindrical structure that mimics the body shape in finite elasticity, obtaining good agreement and understanding for both wild-type and mutant embryos at all stages.

Source connections

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

DAI, A., Ben Amar, M.. 2023-08-15. Cyclic muscle contractions reinforce the acto-myosin motors and mediate the full elongation of C. elegans embryo. https://doi.org/10.1101/2023.08.14.553194

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Lipid-Protein Reciprocal Coupling: A Quantitative Analysis of Membrane Curvature, Architecture, and Protein Association

Cellular membranes are dynamic molecular landscapes in which lipid composition, transbilayer asymmetry, membrane curvature, thickness and mechanics collectively shape protein organization and function, while proteins can in turn remodel lipid organization and membrane architecture. Yet lipid-protein interactions are often treated as discrete binding events, obscuring the extent to which the physical organization of the membrane itself constitutes an active determinant of protein conformational states and cellular activity. Here, we investigate lipid-protein reciprocal coupling by integrating quantitative analyses of curvature-dependent protein-membrane association and hydrophobic-run organization with established structural, lipidomic and biochemical evidence. Our analysis reveals substantial variation in protein association with curved versus flat membrane environments and highlights how membrane curvature, together with lipid composition, cholesterol and asymmetry, can regulate protein structure and function, including in disease-associated systems. We further examine emerging lipid sensors, spatial proteomics and advanced biomimetic membrane platforms that are beginning to bridge molecular mechanisms with protein-lipid organization in cells. In particular, suspended membranes, pore-spanning systems and nanopillar architectures offer opportunities to independently control lipid composition, leaflet asymmetry, curvature and mechanics while directly interrogating protein behaviour. Together, these findings support a model in which membrane architecture encodes physical information that is read by proteins and reciprocally reshaped by protein activity to regulate cellular function.

biophysics↗

A mechanobiological computational framework of intestinal healing for sutureless surgical strategies

Healing of the gastrointestinal (GI) tract following surgical interventions is governed by coupled mechanobiological processes and may lead to severe complications such as perforation or stricture formation. A first comprehensive mechanobiological modeling framework of GI healing is herein proposed. The framework addresses two clinically relevant applications of bioprinting: endoscopic treatment of GI tissue defects and bioprinting-assisted surgical anastomosis. Tissue remodeling is based upon a hyperelastic material model with fiber dispersion coupling the spatiotemporal reaction diffusion dynamics of fibroblasts and cytokines with collagen deposition, reorientation, and plastic deformation. An active stress formulation drives fibroblasts and myofibroblast contraction while a multiplicative decomposition approach is adopted for collagen remodeling as a permanent change. The governing equations are discretised in time with an implicit Euler scheme, finite element in space and solved by a staggered algorithm implemented in the open-source platform FEniCS. Numerical simulations show that the initial collagen fibers content and orientation strongly influence fibroblast infiltration and scar contracture formation. The study quantifies the advantage of having a collagen bioprinted architecture aligned with tissue fibers, to reduce structural remodeling distortion. The model also predicts a strong correlation between collagen deposition and luminal burst pressure during the recovery of mechanical integrity in GI anastomosis.

biophysics↗

Self-centering steady-state flows emerge in confined actomyosin networks

The actin cytoskeleton drives shape changes and transport in cells and supports mechanical signal transmission. However, how cells control and use active cytoskeletal flows at the mesoscale is not well understood. We reconstituted an active cytoskeleton in water-in-oil emulsion droplets of Xenopus laevis egg extract and observed, above a critical droplet size, the emergence of a 3D radially convergent steady-state flow of polymeric actin, maintained by continuous actin turnover. The flow condensed lipid-rich cellular debris into a centered inclusion. Steady-state F-actin density and flow velocity profiles roughly collapse onto scale-invariant master curves. This behavior can be explained by a physical model representing the network as an isotropic active viscous fluid with a percolation threshold. The contracting network behaves as an active swimmer with complex internal dynamics that centers itself and the central inclusion inside the droplets without physical boundary attachment. Active contraction, crosslinking and polymerization dynamics in an actin network can thus generate cell-scale flow patterns that sense the confining geometry and external signals and exert forces that are likely sufficient to move and localize organelles in cells.

biophysics↗