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Molecular and Cellular Biology, May 2009, p. 2346-2358, Vol. 29, No. 9
0270-7306/09/$08.00+0     doi:10.1128/MCB.01233-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Role of the Histone Variant H2A.Z/Htz1p in TBP Recruitment, Chromatin Dynamics, and Regulated Expression of Oleate-Responsive Genes{triangledown}

Yakun Wan,1 Ramsey A. Saleem,1 Alexander V. Ratushny,1 Oriol Roda,1 Jennifer J. Smith,1 Chan-Hsien Lin,1,2 Jung-Hsien Chiang,1,2 and John D. Aitchison1*

Institute for Systems Biology, Seattle, Washington 98103,1 Department of Computer Science and Information Engineering, National Cheng Kung University, Tainan, Taiwan2

Received 5 August 2009/ Returned for modification 9 September 2008/ Accepted 21 January 2009

The histone variant H2A.Z (Htz1p) has been implicated in transcriptional regulation in numerous organisms, including Saccharomyces cerevisiae. Genome-wide transcriptome profiling and chromatin immunoprecipitation studies identified a role for Htz1p in the rapid and robust activation of many oleate-responsive genes encoding peroxisomal proteins, in particular POT1, POX1, FOX2, and CTA1. The Swr1p-, Gcn5p-, and Chz1p-dependent association of Htz1p with these promoters in their repressed states appears to establish an epigenetic marker for the rapid and strong expression of these highly inducible promoters. Isw2p also plays a role in establishing the nucleosome state of these promoters and associates stably in the absence of Htz1p. An analysis of the nucleosome dynamics and Htz1p association with these promoters suggests a complex mechanism in which Htz1p-containing nucleosomes at fatty acid-responsive promoters are disassembled upon initial exposure to oleic acid leading to the loss of Htz1p from the promoter. These nucleosomes reassemble at later stages of gene expression. While these new nucleosomes do not incorporate Htz1p, the initial presence of Htz1p appears to mark the promoter for sustained gene expression and the recruitment of TATA-binding protein.

* Corresponding author. Mailing address: Institute for Systems Biology, 1441 N 34th St., Seattle, WA 98103. Phone: (206) 732-1344. Fax: (206) 732-1299. E-mail: jaitchison{at}systemsbiology.org

{triangledown} Published ahead of print on 9 March 2009.

Molecular and Cellular Biology, May 2009, p. 2346-2358, Vol. 29, No. 9
0270-7306/09/$08.00+0     doi:10.1128/MCB.01233-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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