High impact information on E(bx)

• ATP-dependent histone octamer sliding mediated by the chromatin remodeling complex NURF [1].
• The conservation of NURF in mammals has broad implications for steroid signaling [2].
• To determine in vivo gene targets of NURF, we performed whole genome expression analysis on mutants lacking the NURF-specific subunit NURF301 [2].
• Null Nurf301 mutants do not undergo larval to pupal metamorphosis, and also enhance dominant-negative mutations in ecdysone receptor [2].
• We confirm that NURF is required for transcription activation in vivo [3].

Biological context of E(bx)

• Biological functions of the ISWI chromatin remodeling complex NURF [3].
• Additionally, we show that NURF is required for homeotic gene expression [3].
• Consistent with this, nurf301 mutants recapitulate the phenotypes of Enhancer of bithorax, a positive regulator of the Bithorax-Complex previously localized to the same genetic interval [3].
• NURF is an ISWI complex of four proteins that uses the energy of ATP hydrolysis to catalyze nucleosome sliding [4].
• Isolation of human NURF: a regulator of Engrailed gene expression [5].

Anatomical context of E(bx)

• Finally, mutants in NURF subunits exhibit neoplastic transformation of larval blood cells that causes melanotic tumors to form [3].

Associations of E(bx) with chemical compounds

• An HMGA/HMGI(Y)-like domain of NURF301 that facilitates nucleosome sliding indicates the importance of DNA conformational changes in the sliding mechanism [4].
• To elucidate the mechanism of nucleosome sliding, we have investigated by hydroxyl radical footprinting how NURF makes initial contact with a nucleosome positioned at one end of a DNA fragment [6].
• Alanine scanning mutagenesis demonstrated that H4 residues 16-KRHR-19 are critical for the induction of nucleosome mobility, revealing a histone tail motif that regulates NURF activity [7].
• Alternatively, because accumulation of unhydrolyzed pyrophosphate during nucleotide incorporation inhibits polymerization, NURF may also have been adapted to deliver pyrophosphatase to chromatin to assist in replication or transcription by efficient removal of the inhibitory metabolite [8].
• Inhibition of the pyrophosphatase activity of NURF with sodium fluoride has no significant effect on chromatin remodeling, indicating that these two activities may be biochemically uncoupled [8].

References