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Nat Struct Mol Biol. 2006 Jan;13(1):22-9. Epub 2005 Dec 11.

The human SWI/SNF subunit Brm is a regulator of alternative splicing.

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  • 1Expression Génétique et Maladies, FRE 2850 du CNRS, Département de Biologie du Développement, Institut Pasteur, Paris, France.

Abstract

The SWI/SNF (mating-type switch/sucrose nonfermenting) complex involved in chromatin remodeling on promoters has also been detected on the coding region of genes. Here we show that SWI/SNF can function as a regulator of alternative splicing. We found that the catalytic subunit Brm favors inclusion of variant exons in the mRNA of several genes, including E-cadherin, BIM, cyclin D1 and CD44. Consistent with this, Brm associates with several components of the spliceosome and with Sam68, an ERK-activated enhancer of variant exon inclusion. Examination of the CD44 gene revealed that Brm induced accumulation of RNA polymerase II (RNAPII) with a modified CTD phosphorylation pattern on regions encoding variant exons. Altogether, our data suggest that on genes regulated by SWI/SNF, Brm contributes to the crosstalk between transcription and RNA processing by decreasing RNAPII elongation rate and facilitating recruitment of the splicing machinery to variant exons with suboptimal splice sites.

PMID:
16341228
[PubMed - indexed for MEDLINE]
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