|
|
| Creator |
|
| Examiner |
|
|
|
|
|
| Language |
|
| Academic Year Conferred |
|
| Conferring University |
|
|
|
| Degree |
|
| Degree Type |
|
| Publication Type |
|
| Access Rights |
|
| JaLC DOI |
|
| Related DOI |
|
| Abstract |
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 es...sential 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 (Xist^<CAGΔ5'> ). Xist^<CAGΔ5'> 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 Xist^<CAGΔ5'> 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.show more
|
Export Mendeley
med3065