Polybromo protein BAF180 functions in mammalian cardiac chamber maturation

BAF and PBAF are two related mammalian chromatin remodeling complexes essential for gene expression and development. PBAF, but not BAF, is able to potentiate transcriptional activation in vitro mediated by nuclear receptors, such as RXRalpha, VDR, and PPARgamma. Here we show that the ablation of PBA...

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Bibliographic Details
Published in:Genes & development 2004-12, Vol.18 (24), p.3106-3116
Main Authors: Wang, Zhong, Zhai, Weiguo, Richardson, James A, Olson, Eric N, Meneses, Juanito J, Firpo, Meri T, Kang, Chulho, Skarnes, William C, Tjian, Robert
Format: Article
Language:English
Subjects:
Animals
Cell Aggregation - genetics
Chromatin Assembly and Disassembly - genetics
DNA Primers
DNA-Binding Proteins
Gene Expression Regulation, Developmental
Heart Defects, Congenital - genetics
Heart Defects, Congenital - metabolism
HMGB Proteins
Immunoprecipitation - methods
In Situ Hybridization
In Situ Nick-End Labeling
Mice
Mice, Knockout
Nuclear Proteins - deficiency
Nuclear Proteins - metabolism
Oligonucleotide Array Sequence Analysis
Placenta - abnormalities
Receptors, Retinoic Acid - metabolism
Research Papers
Reverse Transcriptase Polymerase Chain Reaction
S100 Proteins - metabolism
Transcription Factors - deficiency
Transcription Factors - metabolism
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Summary:BAF and PBAF are two related mammalian chromatin remodeling complexes essential for gene expression and development. PBAF, but not BAF, is able to potentiate transcriptional activation in vitro mediated by nuclear receptors, such as RXRalpha, VDR, and PPARgamma. Here we show that the ablation of PBAF-specific subunit BAF180 in mouse embryos results in severe hypoplastic ventricle development and trophoblast placental defects, similar to those found in mice lacking RXRalpha and PPARgamma. Embryonic aggregation analyses reveal that in contrast to PPARgamma-deficient mice, the heart defects are likely a direct result of BAF180 ablation, rather than an indirect consequence of trophoblast placental defects. We identified potential target genes for BAF180 in heart development, such as S100A13 as well as retinoic acid (RA)-induced targets RARbeta2 and CRABPII. Importantly, BAF180 is recruited to the promoter of these target genes and BAF180 deficiency affects the RA response for CRABPII and RARbeta2. These studies reveal unique functions of PBAF in cardiac chamber maturation.
ISSN:0890-9369
1549-5477
DOI:10.1101/gad.1238104