Adenovirus transformation revertant resistant to retransformation by E1 but not by SV40-T and HPV16-E7 oncogenes.
We have previously described a revertant cell line which expresses a dominant tumor suppressor phenotype to E1 but not to heterologous oncogenes such as c-myc, N-ras, or polyoma middle t (Sircar et al. (1988) Oncogene 3, 725-728). DNA tumor virus oncogenes have been suggested to transform cells via the common mechanism of sequestering the Rb-105 antioncoprotein. This paradigm would predict that our revertant cell line, which is resistant to retransformation by E1a, should also be resistant to the other members of the Rb-105 binding family of oncogenes. To test this hypothesis we transfected the revertant cell line with plasmids bearing SV40-T or the HPV16-E7 oncogenes. Because transformation was obtained by both oncogenes at efficiencies similar to the transformation of a related revertant cell line, the results suggest that the resistance phenotype is specific to E1a. This specificity was further confirmed by cell fusion experiments.
Sircar
S
S
Département de microbiologie, Faculté de médecine, Université de Sherbrooke, Québec, Canada.
Horvath
J
J
Roberge
D
D
Diouri
M
M
Weber
J M
JM
D000256:Adenoviridae / Q000235:genetics* / Q000502:physiology; D017500:Adenovirus E1A Proteins / Q000235:genetics / Q000502:physiology*; D000818:Animals; D000952:Antigens, Polyomavirus Transforming / Q000235:genetics / Q000502:physiology*; D002460:Cell Line; D002472:Cell Transformation, Viral; D016153:Genes, Suppressor; D051379:Mice; D009856:Oncogene Proteins, Viral / Q000235:genetics / Q000502:physiology*; D009857:Oncogenes; D050725:Papillomavirus E7 Proteins; D051381:Rats; D013045:Species Specificity
D017500:Adenovirus E1A Proteins; D000952:Antigens, Polyomavirus Transforming; D009856:Oncogene Proteins, Viral; D050725:Papillomavirus E7 Proteins; C059731:oncogene protein E7, Human papillomavirus type 16