Fig. 6: A model describing the receptor complementation mechanism.
From: TGFβ signalling acts as a molecular brake of myoblast fusion
Prior to fusion, myocytes originating from the DML (in orange) express the ligand TGFB3, the effectors SMAD 3, & 4 and the receptor TGFBR1. They are competent to fuse. Myoblasts originating from the posterior or anterior borders of the somite (in blue) express TGFBR2. Upon fusion of myoblasts to DML-derived myocytes, membrane merging of the fusion partners allow the activation of the TGFβ pathway by a receptor heterodimer complementation mechanism (in purple), ultimately leading to a temporary inhibition of fusion of another myoblast. The process of fusion is likely reinitiated after RAB-mediated receptor degradation.
