By Wei Yung Ding1, Hui Ting Ong1, Yusuke Hara1,2, Jantana Wongsantichon3, Yusuke Toyama1,2,4, Robert C. Robinson3,5, François Nédélec6, Ronen Zaidel-Bar1,7
The Journal of Cell Biology. April 2017. doi: 10.1083/jcb.201603070. Epub ahead of print.
The cell cortex is essential to maintain animal cell shape, and contractile forces generated within it by nonmuscle myosin II (NMY-2) drive cellular morphogenetic processes such as cytokinesis. The role of actin cross-linking proteins in cortical dynamics is still incompletely understood. Here, we show that the evolutionarily conserved actin bundling/cross-linking protein plastin is instrumental for the generation of potent cortical actomyosin contractility in the Caenorhabditis elegans zygote. PLST-1 was enriched in contractile structures and was required for effective coalescence of NMY-2 filaments into large contractile foci and for long-range coordinated contractility in the cortex. In the absence of PLST-1, polarization was compromised, cytokinesis was delayed or failed, and 50% of embryos died during development. Moreover, mathematical modeling showed that an optimal amount of bundling agents enhanced the ability of a network to contract. We propose that by increasing the connectivity of the F-actin meshwork, plastin enables the cortex to generate stronger and more coordinated forces to accomplish cellular morphogenesis.
1Mechanobiology Institute, National University of Singapore, Singapore.
2Temasek Life Sciences Laboratory, National University of Singapore, Singapore.
3Institute of Molecular and Cell Biology, A*STAR (Agency for Science, Technology, and Research), Singapore.
4Department of Biological Sciences, National University of Singapore, Singapore.
5Department of Biochemistry, National University of Singapore, Singapore.
6Cell Biology and Biophysics Unit, European Molecular Biology Laboratory, Germany.
7Department of Biomedical Engineering, Faculty of Engineering, National University of Singapore, Singapore.