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* The Lankenau Medical Research Center, Wynnewood, Pennsylvania 19096; and The cell-cell adhesion molecule N-cadherin,
with its associated catenins, is expressed by differentiating skeletal muscle and its precursors. Although N-cadherin's role in later events of skeletal myogenesis such
as adhesion during myoblast fusion is well established,
less is known about its role in earlier events such as
commitment and differentiation. Using an in vitro
model system, we have determined that N-cadherin-
mediated adhesion enhances skeletal muscle differentiation in three-dimensional cell aggregates. We transfected the cadherin-negative BHK fibroblastlike cell
line with N-cadherin. Expression of exogenous N-cadherin upregulated endogenous Department of Biology, University of Toledo,
Toledo, Ohio 43606
-catenin and induced
strong cell-cell adhesion. When BHK cells were cultured as three-dimensional aggregates, N-cadherin enhanced withdrawal from the cell cycle and stimulated differentiation into skeletal muscle as measured by increased expression of sarcomeric myosin and the 12/101
antigen. In contrast, N-cadherin did not stimulate differentiation of BHK cells in monolayer cultures. The
effect of N-cadherin was not unique since E-cadherin also increased the level of sarcomeric myosin in BHK
aggregates. However, a nonfunctional mutant N-cadherin that increased the level of -catenin failed to promote skeletal muscle differentiation suggesting an adhesion-competent cadherin is required. Our results suggest that cadherin-mediated cell-cell interactions
during embryogenesis can dramatically influence skeletal myogenesis.
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