Wild-type p53 is not a negative regulator of simian virus 40 DNA replication in infected monkey cells.
To analyze the proposed growth-inhibitory function of wild-type p53, we compared simian virus 40 (SV40) DNA replication in primary rhesus monkey kidney (PRK) cells, which express wild-type p53, and in the established rhesus monkey kidney cell line LLC-MK2, which expresses a mutated p53 that does not complex with large T antigen. SV40 DNA replication proceeded identically in both cell types during the course of infection. Endogenously expressed wild-type p53 thus does not negatively modulate SV40 DNA replication in vivo. We suggest that inhibition of SV40 DNA replication by wild-type p53 in in vitro replication assays is due to grossly elevated ratios of p53 to large T antigen, thus depleting the replication-competent free large T antigen in the assay mixtures by complex formation. In contrast, the ratio of p53 to large T antigen in in vivo replication is low, leaving the majority of large T antigen in a free, replication-competent state.
Heinrich-Pette-Institut für Experimentelle Virologie und Immunologie, Hamburg, Germany.
A
A
von der Weth
W
W
Deppert
D000818:Animals; D002478:Cells, Cultured; D004261:DNA Replication; D004279:DNA, Viral / Q000096:biosynthesis*; D015536:Down-Regulation; D015967:Gene Expression Regulation, Viral; D016153:Genes, Suppressor / Q000235:genetics*; D008253:Macaca mulatta; D010641:Phenotype; D013539:Simian virus 40 / Q000235:genetics* / Q000254:growth & development; D016159:Tumor Suppressor Protein p53 / Q000502:physiology*
D004279:DNA, Viral; D016159:Tumor Suppressor Protein p53