This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Liu, H. Articles by Zhao, K. Search for Related Content PubMed PubMed Citation Articles by Liu, H. Articles by Zhao, K.

 Previous Article  |  Next Article 

Molecular and Cellular Biology, April 2006, p. 2550-2559, Vol. 26, No. 7
0270-7306/06/$08.00+0     doi:10.1128/MCB.26.7.2550-2559.2006

Cooperative Activity of BRG1 and Z-DNA Formation in Chromatin Remodeling

Laboratory of Molecular Immunology, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892,¹ Laboratory of Molecular Pharmacology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892²

Received 26 September 2005/ Returned for modification 2 December 2005/ Accepted 11 January 2006

The mammalian genome contains tens of thousands of CG and TG repeat sequences that have high potential to form the nonclassical left-handed double-helical Z-DNA structure. Previously we showed that activation of the colony-stimulating factor 1 (CSF1) gene by the chromatin remodeling enzyme, BRG1, results in formation of Z-DNA at the TG repeat sequence located within the promoter. In this report, we show that the TG repeats are assembled in a positioned nucleosome in the silent CSF1 promoter and that activation by BRG1 disrupts this nucleosome and results in Z-DNA formation. Active transcription is not required for the formation of Z-DNA but does result in an expanded region of Z-DNA. Formation of sequences by both BRG1 and the Z-DNA is required for effective chromatin remodeling of the CSF1 promoter. We propose the Z-DNA formation induced by BRG1 promotes a transition from a transient and partial remodeling to a more extensive disruption of the canonical nucleosomal structure. The data presented in this report establish that Z-DNA formation is an important mechanism in modulating chromatin structure, in similarity to the activities of ATP-dependent remodelers and posttranslational histone modifications.

This article has been cited by other articles:

• Khuu, P., Sandor, M., DeYoung, J., Ho, P. S. (2007). Phylogenomic analysis of the emergence of GC-rich transcription elements. Proc. Natl. Acad. Sci. USA 104: 16528-16533 [Abstract] [Full Text]  
• Wong, B., Chen, S., Kwon, J.-A., Rich, A. (2007). Characterization of Z-DNA as a nucleosome-boundary element in yeast Saccharomyces cerevisiae. Proc. Natl. Acad. Sci. USA 104: 2229-2234 [Abstract] [Full Text]  
• Zhang, J., Ohta, T., Maruyama, A., Hosoya, T., Nishikawa, K., Maher, J. M., Shibahara, S., Itoh, K., Yamamoto, M. (2006). BRG1 Interacts with Nrf2 To Selectively Mediate HO-1 Induction in Response to Oxidative Stress. Mol. Cell. Biol. 26: 7942-7952 [Abstract] [Full Text]  
• Morohashi, N., Yamamoto, Y., Kuwana, S., Morita, W., Shindo, H., Mitchell, A. P., Shimizu, M. (2006). Effect of Sequence-Directed Nucleosome Disruption on Cell-Type-Specific Repression by {alpha}2/Mcm1 in the Yeast Genome. Eukaryot Cell 5: 1925-1933 [Abstract] [Full Text]  
• Deigendesch, N., Koch-Nolte, F., Rothenburg, S. (2006). ZBP1 subcellular localization and association with stress granules is controlled by its Z-DNA binding domains. Nucleic Acids Res 34: 5007-5020 [Abstract] [Full Text]