Genetic characterization of mutants resistant to the antiauxin p-chlorophenoxyisobutyric acid reveals that AAR3, a gene encoding a DCN1-like protein, regulates responses to the synthetic auxin 2,4-dichlorophenoxyacetic acid in Arabidopsis roots
Genetic characterization of mutants resistant to the antiauxin p-chlorophenoxyisobutyric acid reveals that AAR3, a gene encoding a DCN1-like protein, regulates responses to the synthetic auxin 2,4-dichlorophenoxyacetic acid in Arabidopsis roots
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DOI：
10.1104/pp.107.104844
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发表时间：
2007-11-01
期刊：
影响因子：
7.4
通讯作者：
Oono, Yutaka
中科院分区：
文献类型：
--
作者：
Biswas, Kamal Kanti;Ooura, Chiharu;Oono, Yutaka
为了分离新的生长素响应突变体在拟南芥（拟南芥），我们筛选突变体根生长抗性的一个假定的antiauxin，对氯苯氧异丁酸（PCIB），抑制生长素的行动，通过干扰上游的生长素信号事件。获得了11株PCIB抗性突变体。遗传作图表明，突变位于至少五个独立的基因座，包括两个已知的生长素相关基因座，运输抑制剂反应1和拟南芥CULLIN 1。抗生长素抗性突变体（阿尔斯）AAR 3 -1、AAR 4和AAR 5也对2，4-二氯苯氧基乙酸具有抗性，如根生长测定所示。aar 3 -1的定位克隆揭示了AAR 3基因编码一个功能未知的蛋白质结构域（DUF 298），该结构域以前没有参与生长素信号传导。该蛋白具有推定的核定位信号，并通过DUF 298结构域与缺陷性库林神经元化-1蛋白具有同源性。结果还表明，PCIB可以促进参与生长素或生长素相关信号转导的因子的鉴定。
To isolate novel auxin-responsive mutants in Arabidopsis (Arabidopsis thaliana), we screened mutants for root growth resistance to a putative antiauxin, p-chlorophenoxyisobutyric acid (PCIB), which inhibits auxin action by interfering the upstream auxin-signaling events. Eleven PCIB-resistant mutants were obtained. Genetic mapping indicates that the mutations are located in at least five independent loci, including two known auxin-related loci, TRANSPORT INHIBITOR RESPONSE1 and Arabidopsis CULLIN1. antiauxin-resistant mutants (aars) aar3-1, aar4, and aar5 were also resistant to 2,4-dichlorophenoxyacetic acid as shown by a root growth assay. Positional cloning of aar3-1 revealed that the AAR3 gene encodes a protein with a domain of unknown function (DUF298), which has not previously been implicated in auxin signaling. The protein has a putative nuclear localization signal and shares homology with the DEFECTIVE IN CULLIN NEDDYLATION-1 protein through the DUF298 domain. The results also indicate that PCIB can facilitate the identification of factors involved in auxin or auxin-related signaling.