Recovery of myc-specific sequences by a partially transformation-defective mutant of avian myelocytomatosis virus, MC29, correlates with the restoration of transforming activity

Abstract

Avian myelocytomatosis virus MC29 transforms fibroblasts and macrophages in vitro. Recently we isolated three deletion mutants of MC29 that have a decreased ability to transform macrophages while retaining their capacity to transform fibroblasts. One of these mutants, MC29 td10H, on passage through chicken embryo cultures gave rise to a recovered virus MC29 10H B1, which has regained the ability to transform macrophages efficiently. Immunoprecipitation analysis of MC29 10H B1-infected cells revealed a 108,000-dalton gag-myc polyprotein as opposed to the 90,000-dalton protein of MC29 td10H or the 110,000-dalton polyprotein of wtMC29. Tryptic peptide mapping studies demonstrated that the 108,000-dalton protein had acquired v-myc peptides that were lost from the td10H 90,000-dalton polyprotein and two novel peptides. Restriction enzyme analysis of the MC29 10H B1 proviral DNA also showed that myc sequences had been acquired. These results suggest that MC29 td10H has recombined with c-myc sequences to generate a recovered virus, MC29 10H B1.