Rous sarcoma virus (RSV) enhancer sequences in the long terminal repeat (LTR) have previously been shown to be sensitive to CpG methylation. We report further that the high density methylation of the RSV LTR-driven chloramphenicol acetyltransferase reporter is needed for full transcriptional inhibition in chicken embryo fibroblasts and for suppression of tumorigenicity of the RSV proviral DNA in chickens. In nonpermissive mammalian cells, however, the low density methylation is sufficient for full inhibition. The time course of inhibition differs strikingly in avian and mammalian cells: although immediately inhibited in mammalian cells, the methylated RSV LTR-driven reporter is fully inhibited with a significant delay after transfection in avian cells. Moreover, transcriptional inhibition can be overridden by transfection with a high dose of the methylated reporter plasmid in chicken cells but not in hamster cells. The LTR, v-src, LTR proviral DNA is easily capable of inducing sarcomas in chickens but not in hamsters. In contrast, Moloney murine leukemia virus LTR-driven v-src induces sarcomas in hamsters with high incidence. Therefore, the repression of integrated RSV proviruses in rodent cells is directed against the LTR.

Institute of Molecular Genetics Academy of Sciences of the Czech Republic Flemingovo nám 2 Prague 6 CZ 16637 Czech Republic

References provided by Crossref.org

The Current View of Retroviruses as Seen from the Shoulders of a Giant

Proviruses with Long-Term Stable Expression Accumulate in Transcriptionally Active Chromatin Close to the Gene Regulatory Elements: Comparison of ASLV-, HIV- and MLV-Derived Vectors

Accumulation of long-term transcriptionally active integrated retroviral vectors in active promoters and enhancers

Role of DNA methylation in expression and transmission of porcine endogenous retroviruses

Transcriptional provirus silencing as a crosstalk of de novo DNA methylation and epigenomic features at the integration site

Epigenetic regulation of transcription and splicing of syncytins, fusogenic glycoproteins of retroviral origin

The core element of a CpG island protects avian sarcoma and leukosis virus-derived vectors from transcriptional silencing

CpG island protects Rous sarcoma virus-derived vectors integrated into nonpermissive cells from DNA methylation and transcriptional suppression