Transformation of rat cells by cyt mutants of adenovirus type 12 and mutants of adenovirus type 5.
Several mutants with much reduced oncogenicity (spontaneous mutants H12 cyt 52 and H12 cyt 70 and UV-induced mutants H12 cyt 61, H12 cyt 62, and H12 cyt 68) of the highly oncogenic adenovirus type 12 (Ad12) were studied for their ability to transform primary baby rat kidney cells. Four of the mutants showed much reduced capacity to transform cells in vitro, while H12 cyt 61 transformed cells as efficiently as the wild-type virus. Viral gene expression in several cell lines established from cultures infected by cyt mutants was studied, and it was found that viral sequences belonging to the left 16% of Ad12 were always transcribed. These results suggest that the function of the transformed state is not defective in the cyt mutants studied. Heterotypic complementation studies showed that the defect(s) in a cyt mutant can be corrected by an Ad7 function. Ad5 dl 313, with a deletion between 3.5 and 10.5 map units, transformed rat cells only at high multiplicity. These results suggest that the region E1B of adenoviruses may be required for efficient transformation of rat cells.
D000260:Adenoviruses, Human / Q000235:genetics* / Q000472:pathogenicity; D000818:Animals; D002472:Cell Transformation, Viral; D002478:Cells, Cultured; D005814:Genes, Viral; D005816:Genetic Complementation Test; D007668:Kidney; D051381:Rats; D014158:Transcription, Genetic