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A more recent version of this article appeared on March 1, 2004
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Submitted on October 15, 2003
Revised on November 26, 2003
Accepted on November 28, 2003
1 Department of Genetics, Stanford University School of Medicine, Stanford, CA 94305-5120
2 Department of Genetics, Stanford University School of Medicine, Stanford, CA 94305-5120, Lewis-Sigler Institute for Integrative Genomics, Princeton University, Princeton, NJ 08544
* Corresponding author. E-mail address: myers{at}shgc.stanford.edu.
Previous work has implicated HSF1 as the primary transcription factor responsible for the transcriptional response to heat stress in mammalian cells. We characterized the heat shock response of mammalian cells by measuring changes in transcript levels and assaying binding of HSF1 to promoter regions for candidate heat shock genes chosen by a combination of genome-wide computational and experimental methods. We found that many heat-inducible genes have HSF1 binding sites (HSE) in their promoters that are bound by HSF1. Surprisingly, for 24 heat-inducible genes, we detected no HSE and no HSF1 binding. Furthermore, of 182 promoters with likely HSE sequences, we detected HSF1 binding at only 94 of these promoters. Also unexpectedly, we found 48 genes with HSEs in their promoters that are bound by HSF1 but which nevertheless did not show induction after heat shock in the cell types we examined. We also studied the transcriptional response to heat shock in fibroblasts from mice lacking the HSF1 gene. We found 36 genes in these cells that are induced by heat as well as they are wild-type cells. These results provide evidence that HSF1 does not regulated the induction of every transcript that accumulates following heat shock, and our results suggest that an independent posttranscriptional mechanism regulates the accumulation of a significant number of transcripts.
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