Myoblast aminophospholipid asymmetry differs from that of fibroblasts

Contemporary theories of fusion processes have focused on the lipids of cell membranes. The dominant rationale for this view is the absence of freezefracture particles at putative fusion sites [1,2], the action of lipophilic reagents as promotors of fusion [3], and the observation that suitably composed lipid vesicles fuse [3,4,5]. Studies of model lipid bilayers specifically implicate two lipids as potentially key molecules in fusion. One of these is PS. Vesicles containing this lipid fuse in the presence of calcium [5,6]. The other major aminophospholipid, PE, forms a hexagonal II-type phase that is reported to be present in fusing cells and is postulated to be an intermediate in that process [7]. The hypothesized role in fusion of these two lipids poses an interesting problem since asymmetry studies O n erythrocytes [8,9] and a cultured mammalian cell line [ 10] indicate a predominantly internal location for these two classes of lipids. The fusion of mononucleate myoblasts into multinucleate myotubes, a key step in the production of muscle fibers provides a convenient system for study-