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• W2482156787 abstract "R. A. Weinberg Massachusetts Institute of Technology Center for Cancer Research and Department of Biology Cambridge, Massachusetts 02139 Introduction SV40 and polyoma are naturally lytic viruses which replicate well in cells derived from their normal hosts. When applied to heterologous cells, these viruses are usually unable to replicate, but may leave a small percentage of the infected cells stably transformed. For example, the monkey virus SV40 is frequently used to transform mouse cells, while the mouse virus polyoma can produce transformed hamster cells. Since papovaviruses normally repli- cate lytically, one assumes that the act of transfor- mation represents expression of a subset of the gene functions which these viruses express during their growth in permissive cells. In this sense, the transformed state represents an abbreviated lytic cycle in which the virus is able to express its early lytic functions without going on to the late phase of viral replication and cell killing. The viral tran- scripts of the early lytic cycle are similar, if not identical to transcripts seen in some transformed cell lines (Weinberg, Ben-lshai and Newbold, 1974; Khoury et al., 1975). The early lytic transcript of these viruses is an mRNA molecule of 19-20s with a length equal to virtually the entire early region of the viral genome (Weinberg and Newbold, 1974; Kamen and Shure, 1976; Turler et al., 1976). Since most, if not all, eucaryotic mRNAs can serve as template for only one polypeptide, the early mRNA might code for only one primary translation product. A large early polypeptide of 90,000-100,000 apparent molecular weight has been found (Tegtmeyer, 1974), but it is unclear whether this protein represents the entire coding capacity of the early mRNA because of diffi- culties in the precise measurement of its molecular weight. The large early protein is precipitable by serum from tumor-bearing animals and therefore carries, among other potential determinants, the T antigen- icity. T antigen is present in almost all tumors de- rived from these viruses, and is also detectable dur- ing the early and late lytic cycle. Its striking nuclear localization and presence in virus-transformed cell lines suggest that it may be the viral transforming protein which acts to transform by binding to a nuclear component, perhaps chromatin. Viral mutations imparting temperature sensitivity for transformation can be localized by marker res- cue experiments to the early portion of the viral genome (Lai and Nathans, 1974, 1975; Mantei, Boyer and Goodman, 1975; Miller and Fried, 1976; Feunteun et al., 1976), and RNA homologous to restriction enzyme fragments from the early region of the viral DNA has been shown to specify the T antigen upon in vitro translation (Prives et al., 1975; Smith et al., 1975; Roberts et al., 1975). Genetic lesions in this part of the genome cause synthesis of thermolabile T antigen (Paulin and Cuzin, 1975; Tenen, Baygell and Livingston, 1975; Kuchino and Yamaguchi, 1975; Alwine et al., 1975). Taken to- gether, these and other experiments (Osborn Weber, 1974) provide strong evidence that the vi- rus-specified T antigen polypeptide, or a related cleavage product, is the viral transforming protein. Such experiments, however, give no insight into the mechanism of transformation. Analysis of the phenotypes of conditional early mutants of these papovaviruses has inspired a wide range of speculations on the mechanism of trans- formation. The A mutants of SV40 and the tsa type polyoma mutants, all of which map in one part of the early region of the viral genome, can be defec- tive in establishment or maintenance of transfor- mation, viral DNA replication and even regulation of early transcription. One might divide these phe- notypes into two classes-those related to the maintenance of the transformed state, and those governing the transcription, replication and per- haps the integration of the viral DNA genome. The temperature-sensitive A type mutations of the SV40 genome have been shown to affect main- tenance of transformation by four groups (Martin and Chou, 1975; Tegtmeyer, Brugge Bu- tel, 1975; Osborn and Weber, 1975). Such experi- ments are performed by deriving transformed clones after infection of mouse cells with these mutants at the permissive low temperature and studying the phenotype of the cloned lines upon subsequent exposure to high temperature. A vari- ety of transformed cell phenotypes are reverted upon shift of A mutant-transformed cells to the nonpermissive temperature. These include serum dependency, colony morphology, 2-deoxyglucose transport, growth in soft agar and actin cable struc- ture. By implication, a viral coded protein is re- quired to maintain the transformed phenotype at permissive temperature. Some of these SV40 A mutants have been shown to have temperature-sensitive functions which can be grouped in a second class-those controlling viral DNA function. These DNA functions are also affected by the tsa polyoma mutation. The most clearly characterized of these functions relates to viral DNA replication. tsa polyoma and tsA SV40 mutants can initiate a normal lytic cycle at permis- sive temperature, and will proceed to replicate viral DNA and express late lytic functions. If the temper- ature is subsequently shifted up, the ongoing viral" @default.
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• W2482156787 date "1977-01-01" @default.
• W2482156787 modified "2023-09-26" @default.
• W2482156787 title "How Does T Antigen Transform Cells? Review" @default.
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