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RESEARCH COMMUNICATION
1 Laboratory of Molecular Cell Biology, National Cancer Institute, NIH, Bethesda, Maryland 20814, USA; 2 Department of Anatomy, Institute of Biomedical Research, University of Birmingham, Edgbaston B15 2TT, United Kingdom; 3 Department of Biology and Center for Genomics and Bioinformatics, Indiana University, Bloomington, Indiana 47405, USA; 4 Whitehead Institute, Massachusetts Institute of Technology, Cambridge, Massachusetts 02142, USA
Drosophila NURF is an ISWI-containing ATP-dependent chromatin remodeling complex that regulates transcription by catalyzing nucleosome sliding. To determine in vivo gene targets of NURF, we performed whole genome expression analysis on mutants lacking the NURF-specific subunit NURF301. Strikingly, a large set of ecdysone-responsive targets is included among several hundred NURF-regulated genes. Null Nurf301 mutants do not undergo larval to pupal metamorphosis, and also enhance dominant-negative mutations in ecdysone receptor. Moreover, purified NURF binds EcR in an ecdysone-dependent manner, suggesting it is a direct effector of nuclear receptor activity. The conservation of NURF in mammals has broad implications for steroid signaling.
[Keywords: NURF; chromatin remodeling; chromatin; Drosophila; Ecdysteroid; ISWI]
Received June 9, 2005; revised version accepted August 26, 2005.
Article and publication are at http://www.genesdev.org/cgi/doi/10.1101/gad.1342605.
6 E-MAIL p.w.badenhorst{at}bham.ac.uk; FAX 44-121-414-3599.
5 E-MAIL carlwu{at}helix.nih.gov; FAX (301) 435-3697.
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Genes & Dev. 2006 20: 2779-2786.
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