X-inactivation is stably maintained in mouse embryos deficient for histone methyl transferase G9a

Tatsuya Ohhata, Makoto Tachibana, Masako Tada, Takashi Tada, Hiroyuki Sasaki, Yoichi Shinkai, Takashi Sado

Research output: Contribution to journalArticlepeer-review

22 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)151-156
Number of pages6
JournalGenesis
Volume40
Issue number3
DOIs
Publication statusPublished - Nov 1 2004
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Genetics
  • Endocrinology
  • Cell Biology

Fingerprint

Dive into the research topics of 'X-inactivation is stably maintained in mouse embryos deficient for histone methyl transferase G9a'. Together they form a unique fingerprint.

Cite this