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Nat Cell Biol. 2017 Aug;19(8):988-995. doi: 10.1038/ncb3577. Epub 2017 Jul 24.

Cortical forces and CDC-42 control clustering of PAR proteins for Caenorhabditis elegans embryonic polarization.

Author information

Temasek Life-sciences Laboratory, 1 Research Link, National University of Singapore, Singapore 117604, Singapore.
Mechanobiology Institute, National University of Singapore, T-Lab, 5A Engineering Drive 1, Singapore 117411, Singapore.
Institute for Molecular and Cell Biology, Agency for Science Technology and Research, 61 Biopolis Drive, Singapore 138673, Singapore.
Department of Biological Sciences, National University of Singapore, 14 Science Drive 4, Singapore 117543, Singapore.


Cell polarization enables zygotes to acquire spatial asymmetry, which in turn patterns cellular and tissue axes during development. Local modification in the actomyosin cytoskeleton mediates spatial segregation of partitioning-defective (PAR) proteins at the cortex, but how mechanical changes in the cytoskeleton are transmitted to PAR proteins remains elusive. Here we uncover a role of actomyosin contractility in the remodelling of PAR proteins through cortical clustering. During embryonic polarization in Caenorhabditis elegans, actomyosin contractility and the resultant cortical tension stimulate clustering of PAR-3 at the cortex. Clustering of atypical protein kinase C (aPKC) is supported by PAR-3 clusters and is antagonized by activation of CDC-42. Cortical clustering is associated with retardation of PAR protein exchange at the cortex and with effective entrainment of advective cortical flows. Our findings delineate how cytoskeleton contractility couples the cortical clustering and long-range displacement of PAR proteins during polarization. The principles described here would apply to other pattern formation processes that rely on local modification of cortical actomyosin and PAR proteins.

[Indexed for MEDLINE]

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