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Molecular and Cellular Biology, June 2004, p. 5249-5256, Vol. 24, No. 12
0270-7306/04/$08.00+0     DOI: 10.1128/MCB.24.12.5249-5256.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Genome-Wide Analysis of the Biology of Stress Responses through Heat Shock Transcription Factor

Ji-Sook Hahn ,1,{dagger},{ddagger} Zhanzhi Hu,2,{dagger} Dennis J. Thiele,1* and Vishwanath R. Iyer2*

Department of Biological Chemistry, University of Michigan Medical School, Ann Arbor, Michigan 48109-0606,1 Institute for Cellular and Molecular Biology and Section of Molecular Genetics and Microbiology, University of Texas at Austin, Austin, Texas 78712-01592

Received 7 November 2003/ Returned for modification 26 January 2004/ Accepted 15 March 2004

Heat shock transcription factor (HSF) and the promoter heat shock element (HSE) are among the most highly conserved transcriptional regulatory elements in nature. HSF mediates the transcriptional response of eukaryotic cells to heat, infection and inflammation, pharmacological agents, and other stresses. While HSF is essential for cell viability in Saccharomyces cerevisiae, oogenesis and early development in Drosophila melanogaster, extended life span in Caenorhabditis elegans, and extraembryonic development and stress resistance in mammals, little is known about its full range of biological target genes. We used whole-genome analyses to identify virtually all of the direct transcriptional targets of yeast HSF, representing nearly 3% of the genomic loci. The majority of the identified loci are heat-inducibly bound by yeast HSF, and the target genes encode proteins that have a broad range of biological functions including protein folding and degradation, energy generation, protein trafficking, maintenance of cell integrity, small molecule transport, cell signaling, and transcription. This genome-wide identification of HSF target genes provides novel insights into the role of HSF in growth, development, disease, and aging and in the complex metabolic reprogramming that occurs in all cells in response to stress.

* Corresponding author. Mailing address for Dennis J. Thiele: Department of Biological Chemistry, University of Michigan Medical School, Ann Arbor, MI 48109-0606. Phone: (919) 684-5776. Fax: (919) 668-6044. E-mail: dennis.thiele{at}duke.edu. Mailing address for Vishwanath R. Iyer: Institute for Cellular and Molecular Biology and Section of Molecular Genetics and Microbiology, University of Texas at Austin, Austin, TX 78712-0159. Phone: (512) 232-7833. Fax: (512) 232-3432. E-mail: vishy{at}mail.utexas.edu.

{dagger} J.-S.H. and Z.H. contributed equally to the work.

{ddagger} Present address: Department of Pharmacology and Cancer Biology and the Sarah W. Stedman Nutrition and Metabolism Center, Duke University Medical Center, Durham, NC 27710.

Molecular and Cellular Biology, June 2004, p. 5249-5256, Vol. 24, No. 12
0022-538X/04/$08.00+0     DOI: 10.1128/MCB.24.12.5249-5256.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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