Differential ability of a T-antigen transport-defective mutant of simian virus 40 to transform primary and established rodent cells.

• DOI: 10.1128/mcb.5.5.1043
• Publication Date: 2015-09-30T19:32:41Z
• Authors: R E Lanford; C Wong; J S Butel
• Keywords: Immunofluorescence

The transforming potential and oncogenicity of a simian virus 40 (SV40) mutant affecting T-antigen (T-ag), SV40(cT)-3, was examined in an effort to dissect T-ag functions transformation. SV40(cT)-3 has point mutation at nucleotide 4434 that abolishes the transport nucleus but does not affect its association with cell surface. Transfection-transformation assays were performed primary cells established lines mouse rat origin. efficiency transformation for by comparable wild-type SV40, indicating can occur absence detectable amounts nuclear T-ag. Transformation embryo fibroblasts markedly influenced culture conditions; relative frequency dramatically reduced involving focus formation low serum concentrations or anchorage-independent growth. Immunofluorescence tests revealed transformed partially cT-ag nucleus. Transformed induced did differ growth properties from transformants. completely defective baby kidney cells, type unable intracellular localization cellular protein p53 found mimic distribution all transformants analyzed. weakly oncogenic vivo: induction tumors newborn hamsters incidence delayed appearance comparison SV40. These observations suggest is regulated both surface-associated forms SV40