Cookies on this website
We use cookies to ensure that we give you the best experience on our website. If you click 'Continue' we'll assume that you are happy to receive all cookies and you won't see this message again. Click 'Find out more' for information on how to change your cookie settings.

In XX female mammals, one of the two X chromosomes is epigenetically inactivated to equalize gene expression with XY males. The formation of the inactive X chromosome (Xi) is regulated by an X-linked long noncoding RNA Xist, which accumulates on the entire length of the chromosome in cis and induces heterochromatin formation. However, the mechanism by which Xist RNA "paints" the Xi has long remained elusive. Here, we show that a matrix protein hnRNP U/SP120/SAF-A is required for the accumulation of Xist RNA on the Xi. Xist RNA and hnRNP U interact and upon depletion of hnRNP U, Xist RNA is detached from the Xi and diffusely localized into the nucleoplasm. In addition, ES cells lacking hnRNP U expression fail to form the Xi. We propose that the association with matrix proteins is an essential step in the epigenetic regulation of gene expression by Xist RNA.

Original publication

DOI

10.1016/j.devcel.2010.08.006

Type

Journal article

Journal

Dev Cell

Publication Date

14/09/2010

Volume

19

Pages

469 - 476

Keywords

Animals, Blotting, Western, Cell Proliferation, Embryo, Mammalian, Female, Fibroblasts, Heterochromatin, Heterogeneous-Nuclear Ribonucleoprotein U, Histones, Immunoenzyme Techniques, In Situ Hybridization, Male, Mice, Neuroblastoma, RNA, Long Noncoding, RNA, Messenger, RNA, Small Interfering, RNA, Untranslated, RNA-Binding Proteins, Reverse Transcriptase Polymerase Chain Reaction, X Chromosome Inactivation