Demethylation of host-cell DNA at the site of avian retrovirus integration
Language English Country United States Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
14623319
DOI
10.1016/j.bbrc.2003.10.035
PII: S0006291X03020990
Knihovny.cz E-resources
- MeSH
- Agar pharmacology MeSH
- Azacitidine analogs & derivatives pharmacology MeSH
- Cell Line MeSH
- CpG Islands MeSH
- Decitabine MeSH
- Transcription, Genetic MeSH
- Genes, src genetics MeSH
- Histone Deacetylases metabolism MeSH
- Enzyme Inhibitors pharmacology MeSH
- Protein Synthesis Inhibitors pharmacology MeSH
- Virus Integration * MeSH
- Terminal Repeat Sequences MeSH
- Cricetinae MeSH
- Mesocricetus MeSH
- Hydroxamic Acids pharmacology MeSH
- DNA Methylation * MeSH
- Models, Genetic MeSH
- Molecular Sequence Data MeSH
- Cell Line, Tumor MeSH
- Retroviridae genetics MeSH
- Sulfites pharmacology MeSH
- Animals MeSH
- Check Tag
- Cricetinae MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Agar MeSH
- Azacitidine MeSH
- Decitabine MeSH
- Histone Deacetylases MeSH
- Enzyme Inhibitors MeSH
- Protein Synthesis Inhibitors MeSH
- Hydroxamic Acids MeSH
- Sulfites MeSH
- trichostatin A MeSH Browser
The transcriptional activity of an integrated retroviral copy strongly depends on the adjacent host-cell DNA at the site of integration. Transcribed DNA loci as well as cis-acting sequences like enhancers or CpG islands usually permit expression of nearby integrated proviruses. In contrast, proviruses residing close to cellular silencers tend to transcriptional silencing and CpG methylation. Little is known, however, about the influence of provirus integration on the target sequence in the host genome. Here, we report interesting features of a simplified Rous sarcoma virus integrated into a non-transcribed hypermethylated DNA sequence in the Syrian hamster genome. After integration, CpG methylation of this sequence has been lost almost completely and hypomethylated DNA permits proviral transcription and hamster cell transformation by the proviral v-src oncogene. This, however, is not a stable state, and non-transformed revertants bearing transcriptionally silenced proviruses segregate with a high rate. The provirus silencing is followed by DNA methylation of both provirus regulatory regions and adjacent cellular sequences. This CpG methylation is very dense and resistant to the demethylation effects of 5-aza-2(')-deoxycytidine and/or trichostatin A. Our description exemplifies the capacity of retroviruses/retroviral vectors to overcome, at least transiently, negative position effects of DNA methylation at the site of integration.
References provided by Crossref.org
The Current View of Retroviruses as Seen from the Shoulders of a Giant
On board a raft or boat in the retrovirus sea
GENBANK
AY243578, AY244357
