Ability of a T-antigen transport-defective mutant of simian virus 40 to immortalize primary cells and to complement polyomavirus middle T in tumorigenesis.
The oncogenic potential of polyomavirus in newborn rats could not be expressed by a genome encoding only the middle T antigen but required the presence of one of the other two viral early genes, small T or large T. The tumorigenicity defect could also be complemented by other viral or cellular genes that are known to be implicated in immortalization and establishment functions. The simian virus 40(cT)-3 mutant (R. E. Lanford and J. S. Butel, Cell 37:801-813, 1984), which fails to localize to the nucleus, has the capacity to complement polyomavirus middle T in tumorigenesis and to immortalize primary rat embryo fibroblasts when it was cotransfected in the presence of pSV2-neo. Our data suggested that under the conditions of DNA-mediated tumor induction and cotransfection with a dominant selection marker, the cellular alterations achieved by nonnuclear oncogenes such as polyomavirus small T and simian virus 40(cT)-3 were sufficient to complement polyomavirus middle T in transformation and tumorigenesis.
D000818:Animals; D000952:Antigens, Polyomavirus Transforming; D000957:Antigens, Viral, Tumor; D002471:Cell Transformation, Neoplastic; D002472:Cell Transformation, Viral; D002478:Cells, Cultured; D005347:Fibroblasts; D009154:Mutation; D009363:Neoplasm Proteins / Q000032:analysis / Q000096:biosynthesis; D009374:Neoplasms, Experimental / Q000209:etiology; D009856:Oncogene Proteins, Viral; D009857:Oncogenes; D010750:Phosphoproteins / Q000032:analysis / Q000096:biosynthesis; D011120:Polyomavirus / Q000276:immunology*; D051381:Rats; D013539:Simian virus 40 / Q000235:genetics / Q000276:immunology*; D014162:Transfection; D016159:Tumor Suppressor Protein p53
D000952:Antigens, Polyomavirus Transforming; D000957:Antigens, Viral, Tumor; D009363:Neoplasm Proteins; D009856:Oncogene Proteins, Viral; D010750:Phosphoproteins; D016159:Tumor Suppressor Protein p53