Satb1 and Satb2 are dispensable for X chromosome inactivation in mice.
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.
Max Planck Institute of Immunobiology and Epigenetics, Department of Cellular and Molecular Immunology, 79108 Freiburg, Germany.
Robert
R
Nechanitzky
Amparo
A
Dávila
Fabio
F
Savarese
Stefanie
S
Fietze
Rudolf
R
Grosschedl
D000818:Animals; D005260:Female; D005347:Fibroblasts / Q000166:cytology / Q000378:metabolism; D036961:Matrix Attachment Region Binding Proteins / Q000172:deficiency* / Q000378:metabolism; D051379:Mice; D014157:Transcription Factors / Q000172:deficiency* / Q000378:metabolism; D049951:X Chromosome Inactivation / Q000235:genetics
D036961:Matrix Attachment Region Binding Proteins; C501473:SATB2 protein, mouse; C469541:Satb1 protein, mouse; D014157:Transcription Factors