Abelson murine leukemia virus mutants deficient in kinase activity and lymphoid cell transformation

Publisher Website
Google Scholar
Abstract
Abelson murine leukemia virus (A-MuLV) transforms mouse lymphoid cells and fibroblasts in vitro and induces a unique type of thymus-independent lymphoma in vivo. Four fibroblast-transforming strains of A-MuLV were identified, based on the sizes of the A-MuLV-specific phosphoproteins produced by these isolates. Two strains, the standard P120- and the P160-producing viruses, transformed lymphoid cells efficiently in vitro and induced Abelson disease in vivo. Two other strains, which synthesized small A-MuLV-specific proteins with MW of 90,000 (P90) and 100,000 (P100), transformed lymphoid cells very poorly in vitro and in vivo. The reduced oncogenic potentials of these isolates were correlated with a high level of synthesis of fairly unstable P90 and P100. Neither P90 nor P100 functioned efficiently in protein kinase assays. The correlation of abnormal metabolism and deficient protein kinase activity with the reduced oncogenic potentials of these virus strains supported a direct role for these proteins and the kinase activity in transformation. Evidently, the requirements for lymphoid cell transformation and fibroblast transformation are different.