Mutations in polyomavirus large T affecting immortalization of primary rat embryo fibroblasts.
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. dl45, dl96, and dl97 have retained the ability to immortalize primary rat embryo fibroblasts and to trans-activate viral promoters. dl8, dl23, and dl300, which are deficient immortalization, are also deficient in transactivation. However, a newly constructed mutant, designated dl141, 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.
Larose
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Department of Microbiology, University of Sherbrooke, Quebec, Canada.
St-Onge
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Bastin
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D000818:Animals; D000957:Antigens, Viral, Tumor / Q000235:genetics / Q000502:physiology*; D002471:Cell Transformation, Neoplastic; D002478:Cells, Cultured; D005091:Exons; D005347:Fibroblasts; D009154:Mutation; D009857:Oncogenes; D011120:Polyomavirus / Q000235:genetics / Q000502:physiology*; D011401:Promoter Regions, Genetic; D051381:Rats; D015533:Transcriptional Activation; D014779:Virus Replication
D000957:Antigens, Viral, Tumor