[
International Worm Meeting,
2011]
Establishment of polarity is essential for conferring different developmental fates to the dividing cells of an embryo. In Caenorhabditis elegans one cell embryos, anteroposterior polarization is facilitated by long-ranged flow of the actomyosin cortex. Even though the flowing cortex contains many actin binding proteins (ABPs) that contribute to its structure and dynamics, there are only a limited number of mechanical properties that are important at large length and time scales relevant for polarization, for example contractility and cortical viscosity (Mayer, Bois, Depken, Julicher, Grill, 2010). Importantly, this suggests that there is only a reduced spectrum of cortical flow phenotypes that one might expect to obtain by modulating these few mechanical properties through different molecular mechanisms. To bridge the gap between molecular and cellular scales, we here sought to investigate which cell-scale mechanical properties are controlled by which ABPs. We devised a candidate RNAi screen of ABPs and found that several ABPs affect cortical flow. This was achieved by analyzing myosin foci size and density and several flow characteristics, such as peak velocities and spatio-temporal velocity-velocity correlations, for each ABP knockdown. The velocity-velocity correlations provided us with an estimation of the characteristic hydrodynamic length of cortical flow, which describes the extent to which flows are long-ranged. Interestingly, all those ABPs that displayed a detectable cortical flow phenotype did so through affecting this hydrodynamic length. RNAi either resulted in short-ranged flows, indicative of a less viscous cortex, or it resulted in flows that were longer-ranged than wild type, indicative of a cortex that is more viscous that under wild-type conditions. Our results suggest that the characteristic hydrodynamic length is a central physical property subject to precise regulation. They also point towards a type of "mechanical redundancy" in animal development, with many molecular mechanisms affecting the same cell-scale physical property.
[
International Worm Meeting,
2015]
During cytokinesis' onset the recruitment of multiple proteins is orchestrated by specific signaling events while reproducible cortical actin flows have been observed. This brings up the question of the contribution of the mechanics during this initial phase of ring assembly. In this study we investigate how myosin induced cortical flows impact actin network organization and filament alignment, thereby directly initiating stable ingression by mechanically remodeling the architecture.We perform our analysis in the early C. elegans zygote. In this organism, a pseudocleavage furrow is formed during the phase of polarizing cortical flows, at a time when the biochemical triggers involved in cytokinesis are not yet present. In this system, we can thus uncouple the mechanical contributions to furrow formation from the biochemical effects involved in the later stages of cytokinesis. We observed that actin filaments align in converging and compressive flow. Hence, alignment and order arises in a disordered network in response to compression by flow and orthogonally to its direction. We show that this partially ingressing furrow is a direct consequence of actin filament alignment induced by the initial flow phase. Quantitative analysis of the dynamics of flows, filaments orientation and cell shape changes, together with theoretical modeling in the framework of a thin film of active and nematic fluid, allowed for a precise characterization of how deformation and shear in the cortical flow gives rise to ordering of actin filaments. Notably, such cortical dynamics and pattern formation arise in a very similar manner both during pseudocleavage and cytokinesis phases.Taken together, our work paints a simple picture of how furrow ingression arises: the presence of a contractility gradient induces the formation of convergent flows, which in turn result in the local alignment of filaments. Filament alignment by compressive flow in turn drives asymmetric stress generation and furrow ingression. We thus identify the key physical principles that lead to the generation of an ingression for cytokinesis.