Journal
DEVELOPMENT
Volume 144, Issue 15, Pages 2784-2797Publisher
COMPANY OF BIOLOGISTS LTD
DOI: 10.1242/dev.149138
Keywords
X chromosome inactivation; Xist RNA; Trophoblast; Mouse; Transcriptome
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Funding
- Ministry of Education, Culture, Sports, Science, and Technology of Japan (MEXT) [26113714, 16H01320, 15K06942, 15H01462, 25116004]
- Grants-in-Aid for Scientific Research [25116004, 17H05606, 16H01320, 16H04739, 15H01462, 17H06426, 26113714, 15K06942] Funding Source: KAKEN
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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 (Xist(CAG Delta 5')). Xist(CAG Delta 5') 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(CAG Delta 5') 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.
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