Satb1 and Satb2 Are Dispensable for X Chromosome Inactivation in Mice

摘要

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. Agrelo et al. previously proposed that Satb family DNA-binding factors allow Xist RNA to initiate X inactivation. Nechanitzky et al. now find that Satb factors are not required for X inactivation and that their expression does not strictly correlate with cellular competence to initiate X inactivation.