| First Author | Sakata Y | Year | 2017 |
| Journal | Development | Volume | 144 |
| Issue | 15 | Pages | 2784-2797 |
| PubMed ID | 28684628 | Mgi Jnum | J:243417 |
| Mgi Id | MGI:5908470 | Doi | 10.1242/dev.149138 |
| Citation | Sakata Y, et al. (2017) Defects in dosage compensation impact global gene regulation in the mouse trophoblast. Development 144(15):2784-2797 |
| abstractText | Xist RNA, which is responsible for X inactivation, is a key epigenetic player in the embryogenesis of female mammals. Of the several repeats conserved in Xist RNA, the A-repeat has been shown to be essential for its silencing function in differentiating embryonic stem cells. Here, we introduced a new Xist allele into mouse that produces mutated Xist RNA lacking the A-repeat (XistCAGDelta5' ). XistCAGDelta5' RNA expressed in the embryo coated the X chromosome but failed to silence it. Although imprinted X inactivation was substantially compromised upon paternal transmission, allele-specific RNA-seq in the trophoblast revealed that XistCAGDelta5' RNA still retained some silencing ability. Furthermore, the failure of imprinted X inactivation had more significant impacts than expected on genome-wide gene expression. It is likely that dosage compensation is required not only for equalizing X-linked gene expression between the sexes but also for proper global gene regulation in differentiated female somatic cells. |
