This study addresses the role of formins at epithelial junctions. A major formin, mDia1, is shown to be recruited to Adherens Junctions (AJs) by E-Cadherin and RhoA. This leads to the organization of actomyosin filaments around the AJs which causes an increase in junctional contractility. Consequently, Tight Junctions (TJs) as well as the epithelial barrier are stabilized.
These findings were published in Cell Reports in 2017.
Acharya BR, Wu SK, Lieu ZZ, Parton RG, Grill SW, Bershadsky AD, Gomez GA, Yap AS. Cell Rep. 2017 Mar 21;18(12):2854-2867. doi: 10.1016/j.celrep.2017.02.078. Mammalian Diaphanous 1 Mediates a Pathway for E-cadherin to Stabilize Epithelial Barriers through Junctional Contractility.
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Figure: mDia1 is required to organize F-actin through RhoA and E-cadherin for effective junctional contractility and subsequent maintenance of epithelial barrier through Tight Junctions (TJs) (Right panel). The left panel shows a leaky epithelial barrier and underlying disorganized actomyosin cytoskeleton on the absence of mDia1 at the AJs.