Protein kinase C mediates the hormonally regulated plasma membrane fusion of avian embryonic skeletal muscle

Recent findings have demonstrated that prostanoid-generated calcium fluxes can trigger myoblast fusion and suggest inositol phospholipid turnover as part of the fusion mechanism. Here we demonstrate that a block imposed on myoblast fusion by antagonists of prostanoid biosynthesis can be overcome by either the membrane-permeable diacylglycerol, 1-oleoyl-2-acetyl-sn-glycerol (OAG), or 12-O-tetradecanoylphorbol 13-acetate (TPA). Both phorbol and the membrane-impermeable dioleoylglycerol were ineffective. These results implicate protein kinase C activation in prostaglandin E1-mediated myoblast fusion and add weight to the contention that inositol turnover is involved in the regulation of myoblast fusion.