HSF3, a new heat shock factor from Arabidopsis thaliana, derepresses the heat shock response and confers thermotolerance when overexpressed in transgenic plants
HSF3, a new heat shock factor from Arabidopsis thaliana, derepresses the heat shock response and confers thermotolerance when overexpressed in transgenic plants
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DOI：
10.1007/s004380050731
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发表时间：
1998-05-01
期刊：
影响因子：
--
通讯作者：
Schöffl, F
中科院分区：
文献类型：
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作者：
Prändl, R;Hinderhofer, K;Schöffl, F
生物体合成热休克蛋白（HSPs），以响应亚致死热应激，并伴随获得对随后的，否则致命的，热休克的耐受性增加。热休克因子（HSF）是许多HSP基因转录所必需的。我们报道了从拟南芥cDNA文库中分离的两个HSF基因，HSF 3和HSF 4。产生含有允许表达HSF 3和HSF 4或各自的翻译β-葡糖醛酸糖苷酶（GUS）融合体的构建体的转基因拟南芥植物。在转基因拟南芥中，HSF3或NSF3-GUS的过表达，而不是HSF4或HSF4-GUS的过表达，导致在25 ℃的非热激温度下HSP的合成。在携带HSF3/HSF3-GUS的转基因植物中，几个热激基因的转录被去抑制。电泳迁移率变动分析表明，热休克反应的去阻遏是由HSF3/HSF3-GUS作为转录因子介导的。HSF3/HSF3-GUS过表达拟南芥植物表现出基础耐热性的增加，表明HSFs和HSF-regulated基因作为热保护过程的决定因素的重要性。转HSF3/HSF3-GUS基因植株没有表现出其它明显的表型改变。过表达后HSF活性的去抑制表明HSF 3的负调节因子或HSF 3的内在组成活性的滴定。我们认为，稳定过表达的热休克因子可能适用于其他生物体作为一种手段，去抑制热休克反应。
Organisms synthesize heat shock proteins (HSPs) in response to sublethal heat stress and concomitantly acquire increased tolerance against a subsequent, otherwise lethal, heat shock. Heat shock factor (HSF) is essential for the transcription of many HSP genes. We report the isolation of two HSF genes, HSF3 and HSF4, from an Arabidopsis cDNA library. Transgenic Arabidopsis plants were generated containing constructs that allow expression of HSF3 and HSF4 or the respective translational beta-glucuronidase (GUS) fusions. Overexpression of HSF3 or NSF3-GUS, but not of HSF4 or HSF4-GUS, causes HSP synthesis at the non-heat-shock temperature of 25 degrees C in transgenic Arabidopsis. In transgenic plants bearing HSF3/HSF3-GUS, transcription of several heat shock genes is derepressed. Electrophoretic mobility shift assays suggest that derepression of the heat shock response is mediated by HSF3/HSF3-GUS functioning as transcription factor. HSF3/HSF3-GUS-overexpressing Arabidopsis plants show an increase in basal thermotolerance, indicating the importance of HSFs and HSF-regulated genes as determinants of thermoprotective processes. Plants transgenic for HSF3/HSF3-GUS exhibit no other obvious phenotypic alterations. Derepression of HSF activity upon overexpression suggests the titration of a negative regulator of HSF3 or an intrinsic constitutive activity of HSF3. We assume that stable overexpression of HSFs may be applied to other organisms as a means of derepressing the heat shock response.