Resistance to retransformation by adenovirus but not by heterologous oncogenes in an E1-positive transformation revertant cell line may be mediated by a cellular function.
Using an indirect selection method based on drug-resistance, we have previously reported the isolation of flat revertants from adenovirus 2 transformed rat cells. Here, we demonstrate that one of these revertants has suffered a mutation in a cellular effector gene specifically required for the adenovirus-mediated expression of the transformed phenotype. Evidence for this conclusion includes the following: (1) the cells contain a 16-times amplified copy of the E1 region, thus reducing the chances of viral mutations, (2) the cells synthesized E1a and E1b proteins indistinguishable from those of the transformed parent, (3) the mutation has been stable for over 2 years, and most importantly (4) the revertant was resistant to re-transformation by E1 but not by c-myc, N-ras or polyoma middle t oncogenes.
Sircar
S
S
Département de Microbiologie, Faculté de Médecine, Centre Hospitalier Universitaire, Sherbrooke, Québec, Canada.
Rodrigues
M
M
Weber
J M
JM
D016475:3T3 Cells; D017500:Adenovirus E1A Proteins / Q000235:genetics / Q000378:metabolism*; D017501:Adenovirus E1B Proteins / Q000235:genetics / Q000378:metabolism*; D000260:Adenoviruses, Human / Q000235:genetics*; D000818:Animals; D002460:Cell Line; D002461:Cell Line, Transformed; D002471:Cell Transformation, Neoplastic; D005814:Genes, Viral; D016259:Genes, myc; D011905:Genes, ras; D051379:Mice; D008819:Mice, Nude; D009857:Oncogenes; D014162:Transfection
D017500:Adenovirus E1A Proteins; D017501:Adenovirus E1B Proteins