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首页> 外文期刊>Molecular and Cellular Biology >The carboxyl-terminal transactivation domain of heat shock factor 1 is negatively regulated and stress responsive.
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The carboxyl-terminal transactivation domain of heat shock factor 1 is negatively regulated and stress responsive.

机译：热休克因子1的羧基末端反式激活结构域是负调控和应力响应。

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摘要

We have characterized a stress-responsive transcriptional activation domain of mouse heat shock factor 1 (HSF1) by using chimeric GAL4-HSF1 fusion proteins. Fusion of the GAL4 DNA-binding domain to residues 124 to 503 of HSF1 results in a chimeric factor that binds DNA yet lacks any transcriptional activity. Transactivation is acquired upon exposure to heat shock or by deletion of a negative regulatory domain including part of the DNA-binding-domain-proximal leucine zippers. Analysis of a collection of GAL4-HSF1 deletion mutants revealed the minimal region for the constitutive transcriptional activator to map within the extreme carboxyl-terminal 108 amino acids, corresponding to a region rich in acidic and hydrophobic residues. Loss of residues 395 to 425 or 451 to 503, which are located at either end of this activation domain, severely diminished activity, indicating that the entire domain is required for transactivation. The minimal activation domain of HSF1 also confers enhanced transcriptional response to heat shock or cadmium treatment. These results demonstrate that the transcriptional activation domain of HSF1 is negatively regulated and that the signal for stress induction is mediated by interactions between the amino-terminal negative regulator and the carboxyl-terminal transcriptional activation domain.
机译：我们已经通过使用嵌合GAL4-HSF1融合蛋白表征了小鼠热激因子1（HSF1）的应力响应转录激活域。 GAL4 DNA结合域与HSF1的124至503位残基的融合产生了一个嵌合因子，该嵌合因子与DNA结合，但缺乏任何转录活性。在暴露于热激下或通过缺失负调节结构域（包括部分DNA结合结构域近端亮氨酸拉链）获得反式激活。 GAL4-HSF1缺失突变体集合的分析揭示了组成型转录激活子在极端羧基末端108个氨基酸内作图的最小区域，对应于一个富含酸性和疏水残基的区域。位于该激活结构域任一端的残基395至425或451至503的丢失严重降低了活性，表明整个结构域是反式激活所必需的。 HSF1的最小激活结构域还赋予热休克或镉处理增强的转录反应。这些结果表明，HSF1的转录激活域受到负调控，而应激诱导的信号是由氨基末端负调控因子与羧基末端转录激活域之间的相互作用介导的。

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