
To investigate the mechanism of cell transformation by the retroviral v-sis gene, we examined the mode of its mRNA expression after infection of primate fibroblasts with Simian Sarcoma Virus (SSV/SSAV). Surprisingly transient expression of the 5.3 kb transcript of v-sis was detected between day two and four after infection. Addition of cycloheximide did not reverse the down-regulation of v-sis expression. Suramin, which uncouples the PDGF receptor complex, had no effect on the pattern of v-sis expression. A marginal but non-transient expression of c-myc and c-fos mRNA upon v-sis expression was detected. Studies on nuclear run-off and m-RNA stability suggest that the half-life time of v-sis mRNA is about 8 h or longer and that its expression is controlled rather by transcriptional than by post-transcriptional mechanisms. The up and down regulation of v-sis expression is independent of the expression of the helper virus (SSAV) gag-genes. This indicates that v-sis oncogene (SSV) and structural genes of the helper virus (SSAV) are obviously under separate expression control.
Oncogene Proteins v-sis, Retroviridae Proteins, Gene Products, gag, Receptors, Cell Surface, Oncogenes, Proto-Oncogene Proteins c-myc, Cell Transformation, Neoplastic, Gene Expression Regulation, Genes, Proto-Oncogene Proteins, Callitrichinae, Animals, Receptors, Platelet-Derived Growth Factor, RNA, Messenger, Cycloheximide, Helper Viruses, Proto-Oncogene Proteins c-fos
Oncogene Proteins v-sis, Retroviridae Proteins, Gene Products, gag, Receptors, Cell Surface, Oncogenes, Proto-Oncogene Proteins c-myc, Cell Transformation, Neoplastic, Gene Expression Regulation, Genes, Proto-Oncogene Proteins, Callitrichinae, Animals, Receptors, Platelet-Derived Growth Factor, RNA, Messenger, Cycloheximide, Helper Viruses, Proto-Oncogene Proteins c-fos
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