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A novel mouse HSF3 has the potential to activate nonclassical heat-shock genes during heat shock

The heat-shock response is characterized by the expression of a set of classical heat-shock genes, and is regulated by heat-shock transcription factor 1 (HSF1) in mammals. However, comprehensive analyses of gene expression have revealed very large numbers of inducible genes in cells exposed to heat...

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Bibliographic Details
Published in:Molecular biology of the cell 2010-01, Vol.21 (1), p.106-116
Main Authors: Fujimoto, Mitsuaki, Hayashida, Naoki, Katoh, Takuma, Oshima, Kouji, Shinkawa, Toyohide, Prakasam, Ramachandran, Tan, Ke, Inouye, Sachiye, Takii, Ryosuke, Nakai, Akira
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Language:English
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Summary:The heat-shock response is characterized by the expression of a set of classical heat-shock genes, and is regulated by heat-shock transcription factor 1 (HSF1) in mammals. However, comprehensive analyses of gene expression have revealed very large numbers of inducible genes in cells exposed to heat shock. It is believed that HSF1 is required for the heat-inducible expression of these genes although HSF2 and HSF4 modulate some of the gene expression. Here, we identified a novel mouse HSF3 (mHSF3) translocated into the nucleus during heat shock. However, mHSF3 did not activate classical heat-shock genes such as Hsp70. Remarkably, overexpression of mHSF3 restored the expression of nonclassical heat-shock genes such as PDZK3 and PROM2 in HSF1-null mouse embryonic fibroblasts (MEFs). Although down-regulation of mHSF3 expression had no effect on gene expression or cell survival in wild-type MEF cells, it abolished the moderate expression of PDZK3 mRNA and reduced cell survival in HSF1-null MEF cells during heat shock. We propose that mHSF3 represents a unique HSF that has the potential to activate only nonclassical heat-shock genes to protect cells from detrimental stresses.
ISSN:1059-1524
1939-4586
DOI:10.1091/mbc.E09-07-0639