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Molecular and Cellular Biology, December 2005, p. 11156-11170, Vol. 25, No. 24
0270-7306/05/$08.00+0     doi:10.1128/MCB.25.24.11156-11170.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Human SWI/SNF Generates Abundant, Structurally Altered Dinucleosomes on Polynucleosomal Templates

Natalia P. Ulyanova and Gavin R. Schnitzler*

Tufts University School of Medicine, Department of Biochemistry, 136 Harrison Ave., Boston, Massachusetts 02111

Received 22 April 2005/ Returned for modification 6 June 2005/ Accepted 22 September 2005

Human SWI/SNF (hSWI/SNF) is an evolutionarily conserved ATP-dependent chromatin remodeling complex required for transcriptional regulation and cell cycle control. The regulatory functions of hSWI/SNF are correlated with its ability to create a stable, altered form of chromatin that constrains fewer negative supercoils than normal. Our current studies indicate that this change in supercoiling is due to the conversion of up to one-half of the nucleosomes on polynucleosomal arrays into asymmetric structures, termed "altosomes," each composed of two histone octamers and bearing an asymmetrically located region of nuclease-accessible DNA. Altosomes can be formed on chromatin containing the abundant mammalian linker histone H1 and have a unique micrococcal nuclease digestion footprint that allows their position and abundance on any DNA sequence to be measured. Over time, altosomes spontaneously revert to structurally normal but improperly positioned nucleosomes, suggesting a novel mechanism for transcriptional attenuation as well as transcriptional memory following hSWI/SNF action.

* Corresponding author. Mailing address: Dept. of Biochemistry, Tufts University School of Medicine, 136 Harrison Ave., Boston, MA 02111. Phone: (617) 636-2441. Fax: (617) 636-2409. E-mail: gavin.schnitzler{at}tufts.edu.

Molecular and Cellular Biology, December 2005, p. 11156-11170, Vol. 25, No. 24
0022-538X/05/$08.00+0     doi:10.1128/MCB.25.24.11156-11170.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Pham, C. D., He, X., Schnitzler, G. R. (2009). Divergent human remodeling complexes remove nucleosomes from strong positioning sequences. Nucleic Acids Res 0: gkp1030v1-gkp1030 [Abstract] [Full Text]  
  • Bouazoune, K., Miranda, T. B., Jones, P. A., Kingston, R. E. (2009). Analysis of individual remodeled nucleosomes reveals decreased histone-DNA contacts created by hSWI/SNF. Nucleic Acids Res 37: 5279-5294 [Abstract] [Full Text]  
  • Sims, H. I., Baughman, C. B., Schnitzler, G. R. (2008). Human SWI/SNF directs sequence-specific chromatin changes on promoter polynucleosomes. Nucleic Acids Res 36: 6118-6131 [Abstract] [Full Text]  
  • Ulyanova, N. P., Schnitzler, G. R. (2007). Inverted Factor Access and Slow Reversion Characterize SWI/SNF-altered Nucleosome Dimers. J. Biol. Chem. 282: 1018-1028 [Abstract] [Full Text]  


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