Abstract:
:The noncoding Xist RNA triggers silencing of one of the two female X chromosomes during X inactivation in mammals. Gene silencing by Xist is restricted to a special developmental context in early embryos and specific hematopoietic precursors. Here, we show that Xist can initiate silencing in a lymphoma model. We identify the special AT-rich binding protein SATB1 as an essential silencing factor. Loss of SATB1 in tumor cells abrogates the silencing function of Xist. In lymphocytes Xist localizes along SATB1-organized chromatin and SATB1 and Xist influence each other's pattern of localization. SATB1 and its homolog SATB2 are expressed during the initiation window for X inactivation in ES cells. Importantly, viral expression of SATB1 or SATB2 enables gene silencing by Xist in embryonic fibroblasts, which normally do not provide an initiation context. Thus, our data establish SATB1 as a crucial silencing factor contributing to the initiation of X inactivation.
journal_name
Dev Celljournal_title
Developmental cellauthors
Agrelo R,Souabni A,Novatchkova M,Haslinger C,Leeb M,Komnenovic V,Kishimoto H,Gresh L,Kohwi-Shigematsu T,Kenner L,Wutz Adoi
10.1016/j.devcel.2009.03.006subject
Has Abstractpub_date
2009-04-01 00:00:00pages
507-16issue
4eissn
1534-5807issn
1878-1551pii
S1534-5807(09)00096-3journal_volume
16pub_type
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