Satb1 and Satb2 Are Dispensable for X Chromosome Inactivation in Mice

SummarySatb1 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.

► Satb1/Satb2 double deficiency is compatible with normal early embryonic development ► Female mice lacking Satb proteins undergo proper dosage compensation ► Female Satb1/Satb2-deficient somatic cells contain a silenced X chromosome ► Satb1/Satb2 expression does not correlate with competence for X inactivation