N-terminally truncated BAF57 isoforms contribute to the diversity of SWI/SNF complexes in neurons.
 

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06-10-09 09:15 AM
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N-terminally truncated BAF57 isoforms contribute to the diversity of SWI/SNF complexes in neurons.
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N-terminally truncated BAF57 isoforms contribute to the diversity of SWI/SNF complexes in neurons.

J Neurochem. 2009 May;109(3):807-18

Authors: Kazantseva A, Sepp M, Kazantseva J, Sadam H, Pruunsild P, Timmusk T, Neuman T, Palm K

The SWItch/Sucrose NonFermentable, a nucleosome remodeling complex (SWI/SNF) chromatin-remodelling complexes act upon the nucleosomal structure and regulate transcription, replication, repair of chromatin and splicing. In this study, we present evidence that human, mouse and rat genes encoding one of the SWI/SNF complex subunits, BAF57, undergo neuron-specific splicing of exons II, III and IV. Alternative splicing yields in at least three isoforms of BAF57 protein that have truncated N-termini (N-BAF57s). The transcripts encoding N-BAF57 isoforms are predominantly expressed in the nervous system. The biochemical fractionation data supported by the results of the co-immunoprecipitation analysis show that N-BAF57 isoforms associate into protein complexes together with Brg1, Brm, BAF155 and BAF170. Transient over-expression of N-BAF57 isoforms in non-neural cells affects the level of expression of certain neuron-restrictive silencer element-containing genes. Together these data suggest that neuronal isoforms of BAF57 contribute to functional SWI/SNF complexes regulating neurogenesis.

PMID: 19245665 [PubMed - indexed for MEDLINE]