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通过应激诱导的聚合作用激活葡萄糖苷酶可迅速增加脱落酸的活性库。

Activation of glucosidase via stress-induced polymerization rapidly increases active pools of abscisic acid.

作者信息

Lee Kwang Hee, Piao Hai Lan, Kim Ho-Youn, Choi Sang Mi, Jiang Fan, Hartung Wolfram, Hwang Ildoo, Kwak June M, Lee In-Jung, Hwang Inhwan

机构信息

Division of Molecular and Life Sciences, Pohang University of Science and Technology, Pohang 790-784, Korea.

出版信息

Cell. 2006 Sep 22;126(6):1109-20. doi: 10.1016/j.cell.2006.07.034.

DOI:10.1016/j.cell.2006.07.034
PMID:16990135
Abstract

Abscisic acid (ABA) is a phytohormone critical for plant growth, development, and adaptation to various stress conditions. Plants have to adjust ABA levels constantly to respond to changing physiological and environmental conditions. To date, the mechanisms for fine-tuning ABA levels remain elusive. Here we report that AtBG1, a beta-glucosidase, hydrolyzes glucose-conjugated, biologically inactive ABA to produce active ABA. Loss of AtBG1 causes defective stomatal movement, early germination, abiotic stress-sensitive phenotypes, and lower ABA levels, whereas plants with ectopic AtBG1 accumulate higher ABA levels and display enhanced tolerance to abiotic stress. Dehydration rapidly induces polymerization of AtBG1, resulting in a 4-fold increase in enzymatic activity. Furthermore, diurnal increases in ABA levels are attributable to polymerization-mediated AtBG1 activation. We propose that the activation of inactive ABA pools by polymerized AtBG1 is a mechanism by which plants rapidly adjust ABA levels and respond to changing environmental cues.

摘要

脱落酸(ABA)是一种对植物生长、发育以及适应各种胁迫条件至关重要的植物激素。植物必须不断调节ABA水平以应对不断变化的生理和环境条件。迄今为止,微调ABA水平的机制仍不清楚。在此我们报道,β-葡萄糖苷酶AtBG1可水解与葡萄糖结合的、无生物活性的ABA以产生活性ABA。AtBG1缺失会导致气孔运动缺陷、种子早萌发、对非生物胁迫敏感的表型以及较低的ABA水平,而异位表达AtBG1的植物积累更高的ABA水平并表现出对非生物胁迫的耐受性增强。脱水迅速诱导AtBG1聚合,导致酶活性增加4倍。此外,ABA水平的昼夜增加归因于聚合介导的AtBG1激活。我们提出,聚合的AtBG1激活无活性的ABA库是植物快速调节ABA水平并响应不断变化的环境信号的一种机制。

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