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The Drosophila Brahma (SWI/SNF) chromatin remodeling complex exhibits cell-type specific activation and repression functions
Journal article   Open access   Peer reviewed

The Drosophila Brahma (SWI/SNF) chromatin remodeling complex exhibits cell-type specific activation and repression functions

Daniel R Marenda, Claudia B Zraly and Andrew K Dingwall
Developmental biology, v 267(2), pp 279-293
15 Mar 2004
DOI: https://doi.org/10.1016/j.ydbio.2003.10.040
PMID: 15013794
Featured in Collection :   UN Sustainable Development Goals @ Drexel
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https://doi.org/10.1016/j.ydbio.2003.10.040View
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Abstract

Immunohistochemistry Wings, Animal - cytology Chromatin Assembly and Disassembly - genetics Drosophila Proteins - metabolism Drosophila melanogaster - genetics Drosophila melanogaster - metabolism Wings, Animal - growth & development Larva - growth & development Larva - genetics Larva - metabolism Cell Cycle Proteins - metabolism DNA Primers Body Patterning - physiology Transcription Factors - metabolism Wings, Animal - metabolism Phenotype Animals Models, Biological Drosophila melanogaster - growth & development Trans-Activators - metabolism Gene Components Body Patterning - genetics Gene Silencing - physiology Chromatin Assembly and Disassembly - physiology Crosses, Genetic
The Brahma (Brm) complex of Drosophila melanogaster is a SWI/SNF-related chromatin remodeling complex required to correctly maintain proper states of gene expression through ATP-dependent effects on chromatin structure. The SWI/SNF complexes are comprised of 8-11 stable components, even though the SWI2/SNF2 (BRM, BRG1, hBRM) ATPase subunit alone is partially sufficient to carry out chromatin remodeling in vitro. The remaining subunits are required for stable complex assembly and/or proper promoter targeting in vivo. Our data reveals that SNR1 (SNF5-Related-1), a highly conserved subunit of the Brm complex, is required to restrict complex activity during the development of wing vein and intervein cells, illustrating a functional requirement for SNR1 in modifying whole complex activation functions. Specifically, we found that snr1 and brm exhibited opposite mutant phenotypes in the wing and differential misregulation of genes required for vein and intervein cell development, including rhomboid, decapentaplegic, thick veins, and blistered, suggesting possible regulatory targets for the Brm complex in vivo. Our genetic results suggest a novel mechanism for SWI/SNF-mediated gene repression that relies on the function of a 'core' subunit to block or shield BRM (SWI2/SNF2) activity in specific cells. The SNR1-mediated repression is dependent on cooperation with histone deacetylases (HDAC) and physical associations with NET, a localized vein repressor.

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Collaboration types
Domestic collaboration
Web of Science research areas
Developmental Biology
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