A novel mouse HSF3 has the potential to activate nonclassical heat-shock genes during heat shock.
A novel mouse HSF3 has the potential to activate nonclassical heat-shock genes during heat shock.
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DOI：
10.1091/mbc.e09-07-0639
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发表时间：
2010-01-01
影响因子：
3.3
通讯作者：
Nakai A
中科院分区：
文献类型：
--
作者：
Fujimoto M;Hayashida N;Katoh T;Oshima K;Shinkawa T;Prakasam R;Tan K;Inouye S;Takii R;Nakai A
HSF 1是哺乳动物细胞热休克反应的主要调节因子，而在禽类细胞中，HSF 3被认为是禽类特异性因子，是经典热休克基因表达所必需的。在这里，作者鉴定了小鼠HSF 3，并证明它具有仅激活非经典热休克基因的潜力。哺乳动物的热休克反应是由一组经典的热休克基因表达的，并受热休克转录因子1（HSF 1）的调控。然而，对基因表达的综合分析揭示了暴露于热休克的细胞中存在大量的诱导基因。据信，HSF1是这些基因的热诱导表达所必需的，尽管HSF2和HSF4调节一些基因表达。在这里，我们确定了一种新的小鼠HSF3（mHSF3）易位到细胞核在热休克。然而，mHSF3没有激活经典的热休克基因，如Hsp70。值得注意的是，mHSF3的过表达恢复了HSF1缺失小鼠胚胎成纤维细胞（MEFs）中非经典热休克基因如PDZK3和PROM2的表达。虽然下调mHSF3表达对野生型MEF细胞中的基因表达或细胞存活没有影响，但它在热休克期间废除了HSF1缺失的MEF细胞中PDZK3 mRNA的适度表达并降低了细胞存活。我们认为mHSF3代表了一种独特的HSF，它有可能只激活非经典的热休克基因，以保护细胞免受有害的压力。
HSF1 is a master regulator of the heat-shock response in mammalian cells, whereas in avian cells, HSF3, which was considered as an avian-specific factor, is required for the expression of classical heat-shock genes. Here, the authors identify mouse HSF3, and demonstrate that it has the potential to activate only nonclassical heat-shock genes. 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.
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影响因子：
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