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The Plant Cuticle Is Required for Osmotic Stress Regulation of Abscisic Acid Biosynthesis and Osmotic Stress Tolerance in Arabidopsis

机译:植物表皮是拟南芥中脱落酸生物合成的渗透胁迫调节和渗透胁迫耐受所必需的

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摘要

Osmotic stress activates the biosynthesis of abscisic acid (ABA). One major step in ABA biosynthesis is the carotenoid cleavage catalyzed by a 9-cis epoxycarotenoid dioxygenase (NCED). To understand the mechanism for osmotic stress activation of ABA biosynthesis, we screened for Arabidopsis thaliana mutants that failed to induce the NCED3 gene expression in response to osmotic stress treatments. The ced1 (for 9-cis epoxycarotenoid dioxygenase defective 1) mutant isolated in this study showed markedly reduced expression of NCED3 in response to osmotic stress (polyethylene glycol) treatments compared with the wild type. Other ABA biosynthesis genes are also greatly reduced in ced1 under osmotic stress. ced1 mutant plants are very sensitive to even mild osmotic stress. Map-based cloning revealed unexpectedly that CED1 encodes a putative α/β hydrolase domain-containing protein and is allelic to the BODYGUARD gene that was recently shown to be essential for cuticle biogenesis. Further studies discovered that other cutin biosynthesis mutants are also impaired in osmotic stress induction of ABA biosynthesis genes and are sensitive to osmotic stress. Our work demonstrates that the cuticle functions not merely as a physical barrier to minimize water loss but also mediates osmotic stress signaling and tolerance by regulating ABA biosynthesis and signaling.
机译:渗透胁迫激活脱落酸(ABA)的生物合成。 ABA生物合成的一个主要步骤是由9-顺式环氧类胡萝卜素双加氧酶(NCED)催化的类胡萝卜素裂解。为了了解ABA生物合成的渗透胁迫激活机制,我们筛选了拟南芥突变体,该突变体未能响应渗透胁迫处理而诱导NCED3基因表达。与野生型相比,本研究中分离的ced1(针对9-顺式环氧类胡萝卜素双加氧酶缺陷1)突变体显示,响应渗透压(聚乙二醇)处理,NCED3的表达显着降低。在渗透胁迫下,ced1中的其他ABA生物合成基因也大大减少。 ced1突变植物甚至对轻度的渗透胁迫也非常敏感。基于图的克隆出乎意料地揭示了CED1编码一个假定的包含α/β水解酶结构域的蛋白质,并与BODYGUARD基因等位基因有关,该基因最近被证明对表皮生物发生至关重要。进一步的研究发现,其他角质生物合成突变体在ABA生物合成基因的渗透胁迫诱导中也受到损害,并且对渗透胁迫敏感。我们的工作表明,角质层不仅起到减少​​水分流失的物理屏障的作用,而且还通过调节ABA的生物合成和信号传导来介导渗透胁迫的信号传导和耐受性。

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