Dynamics of the leaf endoplasmic reticulum modulate β-glucosidase-mediated stress-activated ABA production from its glucosyl ester
Dynamics of the leaf endoplasmic reticulum modulate β-glucosidase-mediated stress-activated ABA production from its glucosyl ester
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DOI：
10.1093/jxb/erz528
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发表时间：
2020-03-25
影响因子：
6.9
通讯作者：
Sakamoto, Atsushi
中科院分区：
文献类型：
--
作者：
Han, Piping;Watanabe, Shunsuke;Sakamoto, Atsushi
植物激素脱落酸（阿坝）是通过多步从头生物合成途径或通过无活性ABA-葡萄糖酯（ABA-GE）的单步水解产生的。水解反应由定位于各种细胞器的β-葡糖苷酶（BG或BGLU）异构体催化，在那里它们在应激时被激活，但这种细胞器特异性激活的机制仍不清楚。我们研究了拟南芥叶片中BGLU 18（BG 1）的亚细胞分布和胁迫诱导的激活之间的关系，BGLU 18是一种对非生物胁迫反应至关重要的内质网酶。高BGLU 18水平存在于叶柄中，主要存在于内质网体中。这些拟南芥特有的内质网衍生的细胞器动态响应非生物胁迫，特别是干旱诱导的脱水，通过改变数量和大小。在胁迫下，BGLU 18的分布向微粒体转移，这是伴随着增加BGLU 18介导的ABA-GE水解活性和阿坝水平的叶柄。在非应激条件下，受损的内质网体形成引起BGLU 18的微粒体移位并增加其酶活性;然而，阿坝水平仅在应激下增加，这可能是因为ABA-GE仅在这些条件下供应给内质网。BGLU 18的缺失延迟了脱水诱导的阿坝积累，表明ABA-GE水解先于生物合成。我们提出内质网的动态调节阿坝的稳态和非生物胁迫反应，通过激活BGLU 18介导的ABA-GE水解。
The phytohormone abscisic acid (ABA) is produced via a multistep de novo biosynthesis pathway or via single-step hydrolysis of inactive ABA-glucose ester (ABA-GE). The hydrolysis reaction is catalyzed by beta-glucosidase (BG, or BGLU) isoforms localized to various organelles, where they become activated upon stress, but the mechanisms underlying this organelle-specific activation remain unclear. We investigated the relationship between the subcellular distribution and stress-induced activation of BGLU18 (BG1), an endoplasmic reticulum enzyme critical for abiotic stress responses, in Arabidopsis thaliana leaves. High BGLU18 levels were present in leaf petioles, primarily in endoplasmic reticulum bodies. These Brassicaceae-specific endoplasmic reticulum-derived organelles responded dynamically to abiotic stress, particularly drought-induced dehydration, by changing in number and size. Under stress, BGLU18 distribution shifted toward microsomes, which was accompanied by increasing BGLU18-mediated ABA-GE hydrolytic activity and ABA levels in leaf petioles. Under non-stress conditions, impaired endoplasmic reticulum body formation caused a microsomal shift of BGLU18 and increased its enzyme activity; however, ABA levels increased only under stress, probably because ABA-GE is supplied to the endoplasmic reticulum only under these conditions. Loss of BGLU18 delayed dehydration-induced ABA accumulation, suggesting that ABA-GE hydrolysis precedes the biosynthesis. We propose that dynamics of the endoplasmic reticulum modulate ABA homeostasis and abiotic stress responses by activating BGLU18-mediated ABA-GE hydrolysis.