| First Author | Ohhata T | Year | 2004 |
| Journal | Genesis | Volume | 40 |
| Issue | 3 | Pages | 151-6 |
| PubMed ID | 15493016 | Mgi Jnum | J:94206 |
| Mgi Id | MGI:3511615 | Doi | 10.1002/gene.20077 |
| Citation | Ohhata T, et al. (2004) X-inactivation is stably maintained in mouse embryos deficient for histone methyl transferase G9a. Genesis 40(3):151-6 |
| abstractText | One of the two X chromosomes becomes inactivated during early development of female mammals. Recent studies demonstrate that the inactive X chromosome is rich in histone H3 methylated at Lys-9 and Lys-27, suggesting an important role for these modifications in X-inactivation. It has been shown that in the mouse Eed is required for maintenance of X-inactivation in the extraembryonic lineages. Interestingly, Eed associates with Ezh2 to form a complex possessing histone methyltransferase activity predominantly for H3 Lys-27. We previously showed that G9a is one of the histone methyltransferases specific for H3 Lys-9 and is essential for embryonic development. Here we examined X-inactivation in mouse embryos deficient for G9a. Expression of Xist, which is crucial for the initiation of X-inactivation, was properly regulated and the inactivated X chromosome was stably maintained even in the absence of G9a. These results demonstrate that G9a is not essential for X-inactivation. genesis 40:151-156, 2004. (c) 2004 Wiley-Liss, Inc. |
