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Transcription factor HAT1 is a substrate of SnRK2.3 kinase and negatively regulates ABA synthesis and signaling in Arabidopsis responding to drought

机译:转录因子HAT1是SnRK2.3激酶的底物并在拟南芥中响应干旱而负调控ABA合成和信号传导

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摘要

Drought is a major threat to plant growth and crop productivity. The phytohormone abscisic acid (ABA) plays a critical role in plant response to drought stress. Although ABA signaling-mediated drought tolerance has been widely investigated in Arabidopsis thaliana, the feedback mechanism and components negatively regulating this pathway are less well understood. Here we identified a member of Arabidopsis HD-ZIP transcription factors HAT1 which can interacts with and be phosphorylated by SnRK2s. hat1hat3, loss-of-function mutant of HAT1 and its homolog HAT3, was hypersensitive to ABA in primary root inhibition, ABA-responsive genes expression, and displayed enhanced drought tolerance, whereas HAT1 overexpressing lines were hyposensitive to ABA and less tolerant to drought stress, suggesting that HAT1 functions as a negative regulator in ABA signaling-mediated drought response. Furthermore, expression levels of ABA biosynthesis genes ABA3 and NCED3 were repressed by HAT1 directly binding to their promoters, resulting in the ABA level was increased in hat1hat3 and reduced in HAT1OX lines. Further evidence showed that both protein stability and binding activity of HAT1 was repressed by SnRK2.3 phosphorylation. Overexpressing SnRK2.3 in HAT1OX transgenic plant made a reduced HAT1 protein level and suppressed the HAT1OX phenotypes in ABA and drought response. Our results thus establish a new negative regulation mechanism of HAT1 which helps plants fine-tune their drought responses.
机译:干旱是对植物生长和作物生产力的主要威胁。植物激素脱落酸(ABA)在植物对干旱胁迫的反应中起关键作用。尽管在拟南芥中已广泛研究了ABA信号介导的干旱耐受性,但对这种途径负调控的反馈机制和成分却知之甚少。在这里,我们确定了一个可以与SnRK2s相互作用并被其磷酸化的拟南芥HD-ZIP转录因子HAT1。 HAT1及其同源物HAT3的功能缺失突变型hat1hat3在初级根抑制,ABA反应基因表达中对ABA高度敏感,并显示出增强的耐旱性,而HAT1过表达株系对ABA敏感性低且对干旱胁迫的耐受性较低提示HAT1在ABA信号介导的干旱反应中起负调控作用。此外,直接与启动子结合的HAT1抑制了ABA生物合成基因ABA3和NCED3的表达水平,导致hat1hat3中ABA水平升高,而HAT1OX系中ABA水平降低。进一步的证据表明,SnRK2.3磷酸化抑制了HAT1的蛋白质稳定性和结合活性。在HAT1OX转基因植物中过表达SnRK2.3使HAT1蛋白水平降低,并抑制ABA和干旱响应中的HAT1OX表型。因此,我们的结果建立了一种新的HAT1负调控机制,可帮助植物微调其干旱反应。

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