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SNR1 (INI1/SNF5) mediates important cell growth functions of the Drosophila Brahma (SWI/SNF) chromatin remodeling complex
Journal article   Open access   Peer reviewed

SNR1 (INI1/SNF5) mediates important cell growth functions of the Drosophila Brahma (SWI/SNF) chromatin remodeling complex

Claudia B Zraly, Daniel R Marenda and Andrew K Dingwall
Genetics (Austin), v 168(1), pp 199-214
Sep 2004
DOI: https://doi.org/10.1534/genetics.104.029439
PMID: 15454538
Featured in Collection :   UN Sustainable Development Goals @ Drexel
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https://doi.org/10.1534/genetics.104.029439View
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Abstract

Cell Growth Processes - physiology Chromatin Assembly and Disassembly - genetics Protein Tyrosine Phosphatases - metabolism Drosophila Proteins - metabolism Drosophila melanogaster - genetics Cyclin-Dependent Kinase 2 Drosophila Proteins - physiology Gene Expression Regulation, Developmental Wings, Animal - anatomy & histology Trans-Activators - genetics Cell Cycle Proteins - genetics G1 Phase - genetics Glutathione Transferase Cell Growth Processes - genetics Transcription Factors - physiology Electrophoresis, Polyacrylamide Gel CDC2-CDC28 Kinases - metabolism Transcription Factors - genetics G1 Phase - physiology Mutation - genetics Reverse Transcriptase Polymerase Chain Reaction Transcription Factors - metabolism Phenotype Animals Fluorescent Antibody Technique Cell Cycle - physiology Drosophila Proteins - genetics
SNR1 is an essential subunit of the Drosophila Brahma (Brm) ATP-dependent chromatin remodeling complex, with counterparts in yeast (SNF5) and mammals (INI1). Increased cell growth and wing patterning defects are associated with a conditional snr1 mutant, while loss of INI1 function is directly linked with aggressive cancers, suggesting important roles in development and growth control. The Brm complex is known to function during G1 phase, where it appears to assist in restricting entry into S phase. In Drosophila, the activity of DmcycE/CDK2 is rate limiting for entry into S phase and we previously found that the Brm complex can suppress a reduced growth phenotype associated with a hypomorphic DmcycE mutant. Our results reveal that SNR1 helps mediate associations between the Brm complex and DmcycE/CDK2 both in vitro and in vivo. Further, disrupting snr1 function suppressed DmcycEJP phenotypes, and increased cell growth defects associated with the conditional snr1E1 mutant were suppressed by reducing DmcycE levels. While the snr1E1-dependent increased cell growth did not appear to be directly associated with altered expression of G1 or G2 cyclins, transcription of the G2-M regulator string/cdc25 was reduced. Thus, in addition to important functions of the Brm complex in G1-S control, the complex also appears to be important for transcription of genes required for cell cycle progression.

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Collaboration types
Domestic collaboration
Web of Science research areas
Genetics & Heredity
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