| First Author | Barakat TS | Year | 2014 |
| Journal | Mol Cell | Volume | 53 |
| Issue | 6 | Pages | 965-78 |
| PubMed ID | 24613346 | Mgi Jnum | J:212497 |
| Mgi Id | MGI:5581575 | Doi | 10.1016/j.molcel.2014.02.006 |
| Citation | Barakat TS, et al. (2014) The trans-activator RNF12 and cis-acting elements effectuate X chromosome inactivation independent of X-pairing. Mol Cell 53(6):965-78 |
| abstractText | X chromosome inactivation (XCI) in female placental mammals is a vital mechanism for dosage compensation between X-linked and autosomal genes. XCI starts with activation of Xist and silencing of the negative regulator Tsix, followed by cis spreading of Xist RNA over the future inactive X chromosome (Xi). Here, we show that XCI does not require physical contact between the two X chromosomes (X-pairing) but is regulated by trans-acting diffusible factors. We found that the X-encoded trans-acting and dose-dependent XCI-activator RNF12 acts in concert with the cis-regulatory region containing Jpx, Ftx, and Xpr to activate Xist and to overcome repression by Tsix. RNF12 acts at two subsequent steps; two active copies of Rnf12 drive initiation of XCI, and one copy needs to remain active to maintain XCI toward establishment of the Xi. This two-step mechanism ensures that XCI is very robust and fine-tuned, preventing XCI of both X chromosomes. |
