Biophysical Society Thematic Meeting | Singapore

Mechanobiology of Disease

Poster Abstracts

58-POS Board 58 Non-Junctional Adhesion-independent E-cadherin Clusters Regulate the Actomyosin Cortex in C.Elegans Zygote Anup Padmanabhan 1 .Ronen Zaidel-Bar 1,2 , 2 National University of Singapore, Singapore, Singapore. 1 Mechanobiology Institute, Singapore, Singapore, During cytokinesis in metazoan cells, the furrow ingression is resisted by intercellular adhesion mediated by cell-cell junctions. Although E-cadherins are best known for their essential role in mediating adhesion at cell junctions, a significant amount of E-cadherin on the cell surface is found outside of cell-cell junctions. The cellular function of these non-junctional cadherin clusters is presently not known. Using live imaging and genetics we show that during in early C. elegans embryos E-cadherin/HMR-1 formed non-junctional puncta at the cell surface associated with cortical F-actin. Depletion of E-cadherin/HMR-1 puncta in 1-cell stage embryo lacking cell- cell junctions accelerated furrow ingression during the first cell division. At the molecular level we observed E-cadherin/HMR-1 and myosinII/NMY-2 to negatively regulate each other and localize to distinct regions both at the cortex and along the ingression furrow. This antagonistic interaction and spatial segregation of E-cadherin/HMR-1 and NMY-2 was dependent on the formin/CYK-1 polymerized F-actin. Finally, we discovered that the non-junctional E- cadherin/HMR-1 puncta localized at the cell surface helps in holding the cortex and membrane together, a hitherto unknown cellular function of non-junctional E-cadherin/HMR-1. Our results thus show that surface localized non-junctional E-cadherin/HMR-1 could regulate cytokinesis beyond its canonical role in inter-cellular adhesion by (1) regulating cortical myosin activity and (2) holding the membrane and cortex together thus resisting cortical deformations such as during furrow ingression.

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