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拟南芥 ADF5 通过调节肌动蛋白细胞骨架重排响应 ABA 和干旱胁迫促进气孔关闭。

Arabidopsis ADF5 promotes stomatal closure by regulating actin cytoskeleton remodeling in response to ABA and drought stress.

机构信息

MOE Key Laboratory of Cell Activities and Stress Adaptations, School of Life Sciences, Lanzhou University, Lanzhou, China.

College of Life Sciences, Zhejiang University, Hangzhou, China.

出版信息

J Exp Bot. 2019 Jan 7;70(2):435-446. doi: 10.1093/jxb/ery385.

Abstract

Stomatal movement plays an essential role in plant responses to drought stress, and the actin cytoskeleton and abscisic acid (ABA) are two important components of this process. Little is known about the mechanism underlying actin cytoskeleton remodeling and the dynamic changes occurring during stomatal movement in response to drought stress/ABA signaling. Actin-depolymerizing factors (ADFs) are conserved actin severing/depolymerizing proteins in eukaryotes, and in angiosperms ADFs have evolved actin-bundling activity. Here, we reveal that the transcriptional expression of neofunctionalized Arabidopsis ADF5 was induced by drought stress and ABA treatment. Furthermore, we demonstrated that ADF5 loss-of-function mutations increased water loss from detached leaves, reduced plant survival rates after drought stress, and delayed stomatal closure by regulating actin cytoskeleton remodeling via its F-actin-bundling activity. Biochemical assays revealed that an ABF/AREB transcription factor, DPBF3, could bind to the ADF5 promoter and activate its transcription via the ABA-responsive element core motif ACGT/C. Taken together, our findings indicate that ADF5 participates in drought stress by regulating stomatal closure, and may also serve as a potential downstream target of the drought stress/ABA signaling pathway via members of the ABF/AREB transcription factors family.

摘要

气孔运动在植物响应干旱胁迫中起着至关重要的作用,肌动蛋白细胞骨架和脱落酸(ABA)是这一过程的两个重要组成部分。目前对于干旱胁迫/ABA 信号转导下肌动蛋白细胞骨架重塑的机制以及气孔运动过程中发生的动态变化知之甚少。肌动蛋白解聚因子(ADFs)是真核生物中保守的肌动蛋白切割/解聚蛋白,在被子植物中,ADFs 进化出了肌动蛋白成束活性。在这里,我们揭示了新功能化的拟南芥 ADF5 的转录表达受干旱胁迫和 ABA 处理诱导。此外,我们还证明,ADF5 功能丧失突变会增加离体叶片的水分损失,降低干旱胁迫后的植物存活率,并通过其 F-肌动蛋白成束活性调节肌动蛋白细胞骨架重塑来延迟气孔关闭。生化分析表明,ABF/AREB 转录因子 DPBF3 可以通过 ABA 反应元件核心基序 ACGT/C 结合到 ADF5 启动子上并激活其转录。综上所述,我们的研究结果表明,ADF5 通过调节气孔关闭参与干旱胁迫,并且可能还通过 ABF/AREB 转录因子家族的成员作为干旱胁迫/ABA 信号通路的潜在下游靶标发挥作用。

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