Biophysical Society Thematic Meeting

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

.Ronen Zaidel-Bar

1,2

National University of Singapore, Singapore, Singapore.

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

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.