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

• Published in: Developmental biology Vol. 267; no. 2; pp. 279 - 293
• Main Authors: Marenda, Daniel R, Zraly, Claudia B, Dingwall, Andrew K
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 15.03.2004
• Subjects: Animals; Body Patterning - genetics; Body Patterning - physiology; Brahma; Cell Cycle Proteins - metabolism; Chromatin; Chromatin Assembly and Disassembly - genetics; Chromatin Assembly and Disassembly - physiology; Crosses, Genetic; Decapentaplegic; DNA Primers; Drosophila melanogaster; Drosophila melanogaster - genetics; Drosophila melanogaster - growth & development; Drosophila melanogaster - metabolism; Drosophila Proteins - metabolism; Gene Components; Gene Silencing - physiology; Immunohistochemistry; Larva - genetics; Larva - growth & development; Larva - metabolism; Models, Biological; Net; Phenotype; Rhomboid; Snr1; SWI/SNF; Thick veins; Trans-Activators - metabolism; Transcription Factors - metabolism; Wing vein development; Wings, Animal - cytology; Wings, Animal - growth & development; Wings, Animal - metabolism; Chromatin; Wing vein development; Thick veins; Decapentaplegic; SWI/SNF; Brahma; Net; Rhomboid; Snr1
• ISSN: 0012-1606; 1095-564X
• DOI: 10.1016/j.ydbio.2003.10.040

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.