Stop us if you’ve heard this one before: new research shows RNA Pol II is a key player in an epigenetic mechanism. Lately, RNA Pol II seems to be in the headlines more than the Jonas Brothers, only with fewer screaming, teen fans.
Recently we featured a paper suggesting that non-coding tiRNAs are formed through Pol II backtracking, and another that highlighted Pol II’s ability to navigate and remodel nucleosomes. Now, Pol II has hit the trifecta as a new study from the National Cancer Center Research Institute in Tokyo has unveiled a link between Pol II binding and CpG Island (CGI) methylation.
The research effort, led by Toshikazu Ushijima, focused on comparative analysis between cancerous promoter methylation and epithelial RNA Pol II engagement in both prostate and breast cancer backgrounds using these techniques:
- MeDIP and CGI microarray hybridization to determine promoter methylation
- RNA Pol II ChIP-on-chip to map out RNA Pol II binding patterns.
By analyzing the data together, they found that Pol II binding, regardless of transcriptional activity, was sufficient to protect promoter CGIs from cancer-induced methylation.