The single cell layer epicardium protects the myocardium at the outer surface of the heart. It is of mesothelial origin and provides growth factors during embryonic heart development. The epicardium is also a source of different types of cardiac cell following the epithelial-mesenchymal transition (EMT). Nonmuscle myosin IIB (NMIIB) regulates tension and contractility of the actin cytoskeleton, and has been shown to be essential for cytokinesis in cardiac myocytes. In this issue (p. 2696), Xuefei Ma, Robert Adelstein and co-workers address the role of NMIIB in epicardial formation and EMT in mice. The authors find that knockout of NMIIB leads to a disruption of epicardial integrity, a loss of E-cadherin at cell−cell junctions and focal detachment of epicardial cells from the myocardium. Furthermore, mesenchymal cell maturation during the epicardial EMT is impaired in these mutants, as the cells fail to properly invade collagen gels. Importantly, knockout of NMIIB, specifically in the epicardium, shows the requirement of NMIIB in the formation of the epicardium for myocardial proliferation and coronary vessel development. Taken together, this work demonstrates a new role for the nonmuscle myosin IIB through the control of the actin cytoskeleton in epicardial function and epicardial EMT during cardiac development.
