CpG methylation suppresses transcriptional activity of human syncytin-1 in non-placental tissues
Language English Country United States Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
16427621
DOI
10.1016/j.yexcr.2005.12.010
PII: S0014-4827(05)00604-X
Knihovny.cz E-resources
- MeSH
- Cell Line MeSH
- CpG Islands physiology MeSH
- Down-Regulation genetics MeSH
- Gene Products, env antagonists & inhibitors biosynthesis genetics MeSH
- HeLa Cells MeSH
- Terminal Repeat Sequences MeSH
- Humans MeSH
- DNA Methylation * MeSH
- Placenta metabolism MeSH
- Promoter Regions, Genetic MeSH
- Pregnancy Proteins antagonists & inhibitors biosynthesis genetics MeSH
- Transcription Factors antagonists & inhibitors biosynthesis genetics MeSH
- Trophoblasts metabolism MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Gene Products, env MeSH
- syncytin MeSH Browser
- Pregnancy Proteins MeSH
- Transcription Factors MeSH
Syncytin-1 is a captive envelope glycoprotein encoded by one of human endogenous retroviruses W. It is expressed exclusively in the placental trophoblast where it participates in cell-to-cell fusion during differentiation of syncytiotrophobast. In other tissues, however, syncytin-1 expression must be kept in check because inadvertent cell fusion might be dangerous for tissue organization and integrity. We describe here an inverse correlation between CpG methylation of syncytin-1 5' long terminal repeat and its expression. Hypomethylation of the syncytin-1 5' long terminal repeat in the placenta and in the choriocarcinoma-derived cell line BeWo was detected. However, other analyzed primary cells and cell lines non-expressing syncytin-1 contain proviruses heavily methylated in this sequence. CpG methylation of syncytin-1 is resistant to the effect of the demethylating agent 5-azacytidine. The inhibitory role of CpG methylation is further confirmed by transient transfection of in-vitro-methylated syncytin-1 promoter-driven reporter construct. Altogether, we conclude that CpG methylation plays a principal role in the transcriptional suppression of syncytin-1 in non-placental tissues, and, in contrast, demethylation of the syncytin-1 promoter in trophoblast is a prerequisite for its expression and differentiation of multinucleated syncytiotrophoblast.
References provided by Crossref.org
Heterologous avian system for quantitative analysis of Syncytin-1 interaction with ASCT2 receptor
The Current View of Retroviruses as Seen from the Shoulders of a Giant
Role of DNA methylation in expression and transmission of porcine endogenous retroviruses
