First Author | Nechanitzky R | Year | 2012 |
Journal | Dev Cell | Volume | 23 |
Issue | 4 | Pages | 866-71 |
PubMed ID | 23079603 | Mgi Jnum | J:330463 |
Mgi Id | MGI:6882166 | Doi | 10.1016/j.devcel.2012.09.018 |
Citation | Nechanitzky R, et al. (2012) Satb1 and Satb2 are dispensable for X chromosome inactivation in mice. Dev Cell 23(4):866-71 |
abstractText | Satb1 and Satb2 have been recently described as regulators of embryonic stem (ES) cell pluripotency and as silencing factors in X chromosome inactivation. The influence of the pluripotency machinery on X chromosome inactivation and the lack of an X chromosome inactivation defect in Satb1(-/-) and Satb2(-/-) mice raise the question of whether or not Satb proteins are directly and/or redundantly involved in this process. Here, we analyzed X chromosome inactivation in fibroblastic cells that were derived from female Satb1(-/-)Satb2(-/-) embryos. By fluorescence in situ hybridization to visualize Xist RNA and by immunohistochemistry to detect H3K27me3 histone modifications, we found that female Satb1(-/-)Satb2(-/-) fibroblastic cells contain proper Barr bodies. Moreover, we did not detect an upregulation of X-linked genes, suggesting that Satb proteins are dispensable for X chromosome inactivation in mice. |