Isolation of Arabidopsis ahg11, a weak ABA hypersensitive mutant defective in nad4 RNA editing.

Isolation of Arabidopsis ahg11, a weak ABA hypersensitive mutant defective in nad4 RNA editing.
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DOI:
10.1093/jxb/ers188
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发表时间:
2012-09
影响因子:
6.9
通讯作者:
Hirayama T
Hirayama T
中科院分区:
生物学1区
文献类型:
--
作者:
Murayama M;Hayashi S;Nishimura N;Ishide M;Kobayashi K;Yagi Y;Asami T;Nakamura T;Shinozaki K;Hirayama T

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植物激素脱落酸(ABA)在植物发育和环境反应的调节中发挥着关键作用。细胞质 ABA 受体的鉴定能够阐明主要的 ABA 信号通路,将 ABA 感知与核事件或几种转运蛋白的作用联系起来。然而,ABA 在细胞过程中的生理功能在很大程度上仍然未知。为了更深入地了解 ABA 反应,进行了遗传筛选以分离拟南芥 ABA 相关突变体,并分离出了几种新型 ABA 超敏感突变体。其中一个突变体——ahg11——得到了进一步的鉴定。基于图谱的克隆表明,AHG11 编码 PPR 型蛋白,该蛋白在 RNA 编辑中具有潜在作用。 AHG11-GFP融合蛋白表明AHG11主要定位于线粒体。与这一观察结果一致,通常进行 RNA 编辑的 nad4 转录物缺乏单个 RNA 编辑事件,导致 ahg11 突变体中氨基酸残基的转换。正在发芽的 ahg11 种子具有更高水平的活性氧反应基因。据推测,复合体 I 成分之一的氨基酸转化导致线粒体功能部分受损,从而引起氧化还原失衡,进而导致对植物激素的异常反应。
The phytohormone abscisic acid (ABA) plays pivotal roles in the regulation of developmental and environmental responses in plants. Identification of cytoplasmic ABA receptors enabled the elucidation of the main ABA signalling pathway, connecting ABA perception to either nuclear events or the action of several transporters. However, the physiological functions of ABA in cellular processes largely remain unknown. To obtain greater insight into the ABA response, genetic screening was performed to isolate ABA-related mutants of Arabidopsis and several novel ABA-hypersensitive mutants were isolated. One of those mutants—ahg11—was characterized further. Map-based cloning showed that AHG11 encodes a PPR type protein, which has potential roles in RNA editing. An AHG11-GFP fusion protein indicated that AHG11 mainly localized to the mitochondria. Consistent with this observation, the nad4 transcript, which normally undergoes RNA editing, lacks a single RNA editing event conferring a conversion of an amino acid residue in ahg11 mutants. The geminating ahg11 seeds have higher levels of reactive-oxygen-species-responsive genes. Presumably, partial impairment of mitochondrial function caused by an amino acid conversion in one of the complex I components induces redox imbalance which, in turn, confers an abnormal response to the plant hormone.
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