| First Author | Sado T | Year | 2000 |
| Journal | Dev Biol | Volume | 225 |
| Issue | 2 | Pages | 294-303 |
| PubMed ID | 10985851 | Mgi Jnum | J:64865 |
| Mgi Id | MGI:1890059 | Doi | 10.1006/dbio.2000.9823 |
| Citation | Sado T, et al. (2000) X inactivation in the mouse embryo deficient for Dnmt1: distinct effect of hypomethylation on imprinted and random X inactivation. Dev Biol 225(2):294-303 |
| abstractText | It has been suggested that DNA methylation plays a crucial role in genomic imprinting and X inactivation. Using DNA methyltransferase 1 (Dnmt1)-deficient mouse embryos carrying X-linked lacZ transgenes, we studied the effects of genomic demethylation on X inactivation. Based on the expression pattern of lacZ, the imprinted X inactivation in the visceral endoderm, a derivative of the extraembryonic lineage, was unaffected in Dnmt1 mutant embryos at the time other imprinted genes showed aberrant expression. Random X inactivation in the embryonic lineage of Dnmt1 mutant embryos, however, was unstable as a result of hypomethylation, causing reactivation of, at least, one lacZ transgene that had initially been repressed. Our results suggest that maintenance of imprinted X inactivation in the extraembryonic lineage can tolerate extensive demethylation while normal levels of methylation are required for stable maintenance of X inactivation in the embryonic lineage. Copyright 2000 Academic Press. |
