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Coronin 1B Reorganizes the Architecture of F-Actin Networks for Contractility at Steady-State and Apoptotic Adherens Junctions

Research output: Contribution to journalArticle

Magdalene Michael, Joyce C.M. Meiring, Bipul R. Acharya, Daniel R. Matthews, Suzie Verma, Siew Ping Han, Michelle M. Hill, Robert G. Parton, Guillermo A. Gomez, Alpha S. Yap

Original languageEnglish
Pages (from-to)58-71
Number of pages14
JournalDevelopmental Cell
Issue number1
Early online date4 Apr 2016
Publication statusE-pub ahead of print - 4 Apr 2016

King's Authors


Summary In this study we sought to identify how contractility at adherens junctions influences apoptotic cell extrusion. We first found that the generation of effective contractility at steady-state junctions entails a process of architectural reorganization whereby filaments that are initially generated as poorly organized networks of short bundles are then converted into co-aligned perijunctional bundles. Reorganization requires coronin 1B, which is recruited to junctions by E-cadherin adhesion and is necessary to establish contractile tension at the zonula adherens. When cells undergo apoptosis within an epithelial monolayer, coronin 1B is also recruited to the junctional cortex at the apoptotic/neighbor cell interface in an E-cadherin-dependent fashion to support actin architectural reorganization, contractility, and extrusion. We propose that contractile stress transmitted from the apoptotic cell through E-cadherin adhesions elicits a mechanosensitive response in neighbor cells that is necessary for the morphogenetic event of apoptotic extrusion to occur.

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