| First Author | Kamikawa YF | Year | 2015 |
| Journal | PLoS One | Volume | 10 |
| Issue | 5 | Pages | e0125626 |
| PubMed ID | 25993097 | Mgi Jnum | J:235416 |
| Mgi Id | MGI:5796253 | Doi | 10.1371/journal.pone.0125626 |
| Citation | Kamikawa YF, et al. (2015) Histone demethylation maintains Prdm14 and Tsix expression and represses xIst in embryonic stem cells. PLoS One 10(5):e0125626 |
| abstractText | Epigenetic reprogramming is exemplified by the remarkable changes observed in cellular differentiation and X-chromosome inactivation (XCI) in mammalian female cells. Histone 3 lysine 27 trimethylation (H3K27me3) is a modification that suppresses gene expression in multiple contexts including embryonic stem cells (ESCs) and decorates the entire inactive X-chromosome. The conversion of female somatic cells to induced pluripotency is accompanied by X-chromosome reactivation (XCR) and H3K27me3 erasure. Here, we show that the H3K27-specific demethylase Utx regulates the expression of the master regulators for XCI and XCR: Prdm14, Tsix, and Xist. Female ESC transcriptome analysis using a small molecule inhibitor for H3K27 demethylases, GSK-J4, identifies novel targets of H3K27 demethylation. Consistent with a recent report that GSK-J4 can inhibit other histone demethylase, we found that elevated H3K4me3 levels are associated with increased gene expression including Xist. Our data suggest multiple regulatory mechanisms for XCI via histone demethylation. |
