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Abstract


The available genetic data, although still not conclusive, continue to suggest that transformation by polyoma virus is mediated entirely by middle T antigen (see below), whereas that brought about by SV40 is mediated by large T antigen, with assistance in some cases from small T antigen (Seif and Martin 1979a; Topp and Rifkin 1980). Thus, transforming activity is carried only by fragments of SV40 DNA that span the entire early region of the viral genome (Graessmann et al. 1980); all SV40 transformants so far analyzed contain a functional gene for large T antigen. In contrast, transformed cells and tumors induced by polyoma virus do not always contain the entire coding sequence for large T antigen; however, they invariably retain and express only that segment of the early region that codes for small T and middle T antigens (Birg et al. 1979; Lania et al. 1980). Accordingly, both transformants and tumors can be obtained by introducing into cells or animals merely those segments of viral DNA that span the proximal portion of the early region but lack the sequences coding for the distal portion of large T antigen (Chowdhury et al. 1980; Hassell et al. 1980; Novak et al. 1980).

There is little significant advance in our understanding of how these viral proteins translate the cell into a transformed state and maintain it there. Some laboratories continue to report that cells transformed by tsA mutants of polyoma virus or SV40 show no change in phenotype after they are shifted to nonpermissive...


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DOI: http://dx.doi.org/10.1101/0.296a-296g