Abstract
XIST
RNA triggers the transformation of an active X chromosome into a condensed, inactive Barr body and therefore provides a unique window into transitions of higher-order chromosome architecture. Despite recent progress, how
XIST
RNA localizes and interacts with the X chromosome remains poorly understood. Genetic engineering of
XIST
into a trisomic autosome demonstrates remarkable capacity of
XIST
RNA to localize and comprehensively silence that autosome. Thus,
XIST
does not require X chromosome-specific sequences but operates on mechanisms available genome-wide. Prior results suggested
XIST
localization is controlled by attachment to the insoluble nuclear scaffold. Our recent work affirms that scaffold attachment factor A (SAF-A) is involved in anchoring
XIST
, but argues against the view that SAF-A provides a unimolecular bridge between RNA and the chromosome. Rather, we suggest that a complex meshwork of architectural proteins interact with
XIST
RNA. Parallel work studying the territory of actively transcribed chromosomes suggests that repeat-rich RNA ‘coats’ euchromatin and may impact chromosome architecture in a manner opposite of
XIST
. A model is discussed whereby RNA may not just recruit histone modifications, but more directly impact higher-order chromatin condensation via interaction with architectural proteins of the nucleus.
This article is part of the themed issue ‘X-chromosome inactivation: a tribute to Mary Lyon’.
Funder
National Institute of General Medicine
Subject
General Agricultural and Biological Sciences,General Biochemistry, Genetics and Molecular Biology
Cited by
38 articles.
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