[대학원 생명과학과 세미나 안내]

 

연사 : 최왕선 박사 (Brigham and Women’s Hospital and Harvard Medical School)


연제 : How to build a cellular tension at nanoscale: a super-resolution view

 

일시 : 2016년 6월 27일 (월오후 4

 

장소 하나과학관 A동 307


초청교수 : 최의주 교수


Abstract


Morphogenesis and epithelial homeostasis require dynamic coordination between cell-cell adhesion and cytoskeletal tension at cell-cell junctions. In the past decade, it has become increasingly clear that the textbook view of the cell-cell zonula adherens (ZA), as a static ring of transmembrane cadherins linked to an underlying ring of actin and myosin via catenins, is misleading. Here we addressed two key questions in the field:  how do cells maintain epithelial integrity under tension and how are cell junctions remodeled in response to tension to ensure this. We used super-resolution microscopy, tension-sensing antibodies, and nanoscale laser ablation to define the architecture of junctions and the cytoskeleton under tension in molecular detail, and to determine how changes in individual cells alter the architecture and properties of the entire epithelial sheet. When cells undergo an increase in contractility, the architecture of actin and myosin at the ZA remodels into a contractile array at the bi-cellular contacts with the actin cables anchored end on into cadherin complexes at tricellular junctions. We found that Rho-dependent kinase (ROCK) and Shroom3 proteins promotes the increase in contractility whereas ZO family proteins normally suppress actomyosin contractility at the ZA. We also found a striking role for afadin which regulates the uniform distribution of actomyosin units at cell-cell contacts in response to increased tension. Our findings refine the roles of key scaffolding proteins in organizing and anchoring junctions in epithelia.