The suppression of WRKY44 by GIGANTEA-miR172 pathway is involved in drought response of Arabidopsis thaliana.
The suppression of WRKY44 by GIGANTEA-miR172 pathway is involved in drought response of Arabidopsis thaliana.
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DOI：
10.1371/journal.pone.0073541
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发表时间：
2013
期刊：
影响因子：
3.7
通讯作者：
Ming F
中科院分区：
文献类型：
--
作者：
Han Y;Zhang X;Wang W;Wang Y;Ming F
水分供应是控制开花时间的重要环境因素。许多植物在干旱条件下加速开花，这种现象称为干旱逃逸。四种途径参与控制开花时间，但哪些参与干旱逃逸尚不清楚。在这项研究中，具有GIGANTEA（GI）和CONSTANS（CO）功能丧失突变的植物表现出异常的干旱逃避表型。干旱胁迫下，GI和FKF 1（Flavin-binding Kelch domain F box protein 1）的mRNA表达峰值以及CO和FT（Flowering locus T）的mRNA表达水平发生变化。microRNA因子miRNA 172 E在干旱胁迫下表达上调，且其表达上调依赖于GI，而其他miRNA 172 s表达上调不依赖于GI。水分损失分析表明，gi突变体对干旱胁迫更敏感，而miRNA 172过表达（miRNA 172-OX）植株对干旱胁迫的敏感性低于野生型植株。数字基因表达和实时PCR分析表明，WRKY 44被GI和miRNA 172下调。WRKY 44蛋白在酵母双杂交系统中可与miRNA 172的靶基因TOE 1相互作用。我们推测GI-miRNA 172-WRKY 44可能通过影响糖信号通路来调节拟南芥的干旱逃逸和耐旱性。
Water availability is an important environmental factor that controls flowering time. Many plants accelerate flowering under drought conditions, a phenomenon called drought escape. Four pathways are involved in controlling flowering time, but which ones participate in drought escape is not yet known. In this study, plants with loss-of-function mutations of GIGANTEA (GI) and CONSTANS (CO) exhibited abnormal drought-escape phenotypes. The peak mRNA levels of GI and FKF1 (Flavin-binding Kelch domain F box protein 1) and the mRNA levels of CO and FT (Flowering locus T) changed under drought stress. The microRNA factor miRNA172E was up-regulated by drought stress, and its up-regulation was dependent on GI, while other miRNA172s were not. Water-loss analyses indicated that gi mutants were more sensitive while miRNA172 over-expressing (miRNA172-OX) plants were less so to drought stress than wild-type plants. Digital gene expression and real-time PCR analyses showed that WRKY44 was down-regulated by GI and miRNA172. The WRKY44 protein could interact with TOE1 (a target of miRNA172) in a yeast two-hybrid system. We proposed that GI–miRNA172–WRKY44 may regulate drought escape and drought tolerance by affecting sugar signaling in Arabidopsis.
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