Biotechnology Center, Technical University Dresden, Dresden, Germany; Max Planck Institute for the Physics of Complex Systems, Dresden, Germany; Max Planck Institute of Molecular Cell Biology and Genetics, Dresden, Germany
Sundar Ram Naganathan
Biotechnology Center, Technical University Dresden, Dresden, Germany; Max Planck Institute for the Physics of Complex Systems, Dresden, Germany; Max Planck Institute of Molecular Cell Biology and Genetics, Dresden, Germany
Biotechnology Center, Technical University Dresden, Dresden, Germany; Max Planck Institute for the Physics of Complex Systems, Dresden, Germany; Max Planck Institute of Molecular Cell Biology and Genetics, Dresden, Germany
The actomyosin cell cortex is an active contractile material for driving cell- and tissue morphogenesis. The cortex has a tendency to form a pattern of myosin foci, which is a signature of potentially unstable behavior. How a system that is prone to such instabilities can rveliably drive morphogenesis remains an outstanding question. Here, we report that in the Caenorhabditis elegans zygote, feedback between active RhoA and myosin induces a contractile instability in the cortex. We discover that an independent RhoA pacemaking oscillator controls this instability, generating a pulsatory pattern of myosin foci and preventing the collapse of cortical material into a few dynamic contracting regions. Our work reveals how contractile instabilities that are natural to occur in mechanically active media can be biochemically controlled to robustly drive morphogenetic events.
