A small deletion in the carboxy terminus of the viral myc gene renders the virus MC29 partially transformation defective in avian fibroblasts.

In order to characterize the role of the carboxy terminus of the viral myc protein in the transformation of avian fibroblasts and macrophages, several Bal31 deletion mutants were created which removed varying portions of the carboxy terminus of the myc protein. Only one such mutant, S90.9, which had lost nine amino acids of myc retained biological activity when tested in macrophages and fibroblasts. This mutant transformed avian macrophages in a manner similar to that of wild-type, but appeared to be partially transformation defective in fibroblasts. Chicken embryo fibroblast cultures infected with S90.9 exhibited an intermediate phenotype morphologically when compared to wild-type-infected cells. When tested for growth in soft agar, the presence or absence of actin cables and fibronectin on the cell surface, and growth rate, S90.9-infected cells showed intermediate behavior when compared to wild-type or helper virus-infected fibroblasts. These experiments suggest that the carboxy terminus of the myc protein, which is highly basic in nature, is involved in the transformation of avian fibroblasts.