title: Mechanism of murine leukemia virus-induced fusion in rat myoblasts defective in differentiation.
abstract: fu-1 cells, a line of rat myoblasts defective in differentiation, can be fused into multinucleate syncytia by Moloney murine leukemia virus. The effects of treating the virus with specific antibody, UV irradiation, and elevated temperature and the requirements for cellular RNA and protein synthesis have been studied as they relate to this virus-induced fusion. The results indicate that intact, but not necessarily infectious, virions are required to promote fusion of fu-1 cells. Neither actinomycin D nor cycloheximide altered the formation of syncytia; thus, neither viral nor cellular RNA or protein synthesis is required for fusion. fu-1 cells infected with the ts3 temperature-sensitive mutant of Moloney murine leukemia virus accumlate large amounts of budding  virus on their cell membrane; however, this membrane-associated virus failed to induce syncytia. Upon release of the virus at the permissive temperature, fusion did occur. We conclude that contact or attachment of the immature virus to the cell membrane is not sufficient to promote murine leukemia virus-induced cell fusion; complete virions are required. From these data, we propose that adsorption and penetration of the virus may induce a change in the cell membrane that subsequently promotes the fusion of susceptible cells.
mesh_terms: D000818:Animals; D002459:Cell Fusion / Q000187:drug effects; D002460:Cell Line; D003513:Cycloheximide / Q000494:pharmacology; D003609:Dactinomycin / Q000494:pharmacology; D006358:Hot Temperature; D007106:Immune Sera / Q000494:pharmacology; D008979:Moloney murine leukemia virus / Q000187:drug effects / Q000254:growth & development* / Q000528:radiation effects; D009132:Muscles; D009154:Mutation; D051381:Rats; D013696:Temperature; D014466:Ultraviolet Rays; D014779:Virus Replication
chemical_list: D007106:Immune Sera; D003609:Dactinomycin; D003513:Cycloheximide