A frameshift at a mutational hotspot in the polyoma virus early region generates two new proteins that define T-antigen functional domains.
A frameshift mutation, arising from the deletion of any one of nine consecutive cytidines in the region of Py DNA encoding both the midregion of large T-Ag and the C-terminal region of middle T-Ag, yields unstable flat cell revertants that synthesize two novel viral proteins in which shuffling of the different domains of the Py T-Ags has occurred. The first protein (37 kd) is a hybrid containing the N-terminus of large T-Ag and the hydrophobic C-terminus of middle T-Ag. The latter domain is responsible for membrane association, even in the 37 kd hybrid protein. The second protein (43 kd), which contains the N-terminal 75% of middle T-Ag, has an associated protein kinase activity and forms a complex with c-src, but cannot induce a transformed phenotype.
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JB
Wilson
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Hayday
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Courtneidge
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Fried
D000818:Animals; D000957:Antigens, Viral, Tumor / Q000235:genetics* / Q000276:immunology; D002460:Cell Line; D002462:Cell Membrane / Q000276:immunology; D002471:Cell Transformation, Neoplastic; D002472:Cell Transformation, Viral; D003593:Cytoplasm / Q000276:immunology; D000939:Epitopes / Q000276:immunology; D005814:Genes, Viral; D009154:Mutation; D010641:Phenotype; D011120:Polyomavirus / Q000201:enzymology / Q000235:genetics* / Q000276:immunology; D011494:Protein Kinases / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics; D051381:Rats
D000957:Antigens, Viral, Tumor; D000939:Epitopes; D012333:RNA, Messenger; D011494:Protein Kinases