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热诱导转录因子 HsfA2 增强拟南芥的缺氧耐受能力。

The heat-inducible transcription factor HsfA2 enhances anoxia tolerance in Arabidopsis.

机构信息

Plant Lab, Scuola Superiore Sant'Anna, 56127 Pisa, Italy.

出版信息

Plant Physiol. 2010 Mar;152(3):1471-83. doi: 10.1104/pp.109.149815. Epub 2010 Jan 20.

DOI:10.1104/pp.109.149815
PMID:20089772
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2832282/
Abstract

Anoxia induces several heat shock proteins, and a mild heat pretreatment can acclimatize Arabidopsis (Arabidopsis thaliana) seedlings to subsequent anoxic treatment. In this study, we analyzed the response of Arabidopsis seedlings to anoxia, heat, and combined heat + anoxia stress. A significant overlap between the anoxic and the heat responses was observed by whole-genome microarray analysis. Among the transcription factors induced by both heat and anoxia, the heat shock factor A2 (HsfA2), known to be involved in Arabidopsis acclimation to heat and to other abiotic stresses, was strongly induced by anoxia. Heat-dependent acclimation to anoxia is lost in an HsfA2 knockout mutant (hsfa2) as well as in a double mutant for the constitutively expressed HsfA1a/HsfA1b (hsfA1a/1b), indicating that these three heat shock factors cooperate to confer anoxia tolerance. Arabidopsis seedlings that overexpress HsfA2 showed an increased expression of several known targets of this transcription factor and were markedly more tolerant to anoxia as well as to submergence. Anoxia failed to induce HsfA2 target proteins in wild-type seedlings, while overexpression of HsfA2 resulted in the production of HsfA2 targets under anoxia, correlating well with the low anoxia tolerance experiments. These results indicate that there is a considerable overlap between the molecular mechanisms of heat and anoxia tolerance and that HsfA2 is a player in these mechanisms.

摘要

缺氧诱导产生多种热休克蛋白,轻度热预处理可使拟南芥(Arabidopsis thaliana)幼苗适应随后的缺氧处理。在本研究中,我们分析了拟南芥幼苗对缺氧、热和热+缺氧联合胁迫的反应。通过全基因组微阵列分析,观察到缺氧和热反应之间存在显著重叠。在热和缺氧均诱导的转录因子中,热休克因子 A2(HsfA2)强烈诱导缺氧,已知其参与拟南芥对热和其他非生物胁迫的适应。在 hsfA2 敲除突变体(hsfa2)和组成型表达 HsfA1a/HsfA1b(hsfA1a/1b)的双突变体中,热依赖性的缺氧适应丧失,表明这三种热休克因子合作赋予了缺氧耐受性。过表达 HsfA2 的拟南芥幼苗表现出该转录因子的几个已知靶标表达增加,对缺氧和淹没的耐受性明显增强。在野生型幼苗中,缺氧未能诱导 HsfA2 靶蛋白的产生,而过表达 HsfA2 导致在缺氧条件下产生 HsfA2 靶标,与低缺氧耐受性实验结果很好地相关。这些结果表明,热和缺氧耐受性的分子机制之间存在相当大的重叠,HsfA2 是这些机制中的一个参与者。

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