Mutations in polyomavirus large T affecting immortalization of primary rat embryo fibroblasts

Abstract

To clarify the relationship between various functions of the polyomavirus large T antigen and the contribution of this oncogene toward neoplastic transformation, we have analyzed the properties of mutants with in-frame deletions in the second large T exon. d/45, d/96, and d/97 have retained the ability to immortalize primary rat embryo fibroblasts and to trans-activate viral promoters. d/8, d/23, and d/300, which are deficient in immortalization, are also deficient in trans-activation. However, a newly constructed mutant, designated d/141, which is deficient in immortalization, is still able to trans-activate both the polyoma and SV40 late promoters. This indicates that the ability to trans-activate promoters is not sufficient to confer on the large T antigen the ability to immortalize primary cells.