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微小RNA393通过支架蛋白1型受体激活蛋白激酶C1A介导的脱落酸信号通路调控拟南芥的盐胁迫响应途径。

miR393s regulate salt stress response pathway in Arabidopsis thaliana through scaffold protein RACK1A mediated ABA signaling pathways.

作者信息

Denver Jn Baptiste, Ullah Hemayet

机构信息

a Department of Biology , Howard University , Washington , DC , USA.

出版信息

Plant Signal Behav. 2019;14(6):1600394. doi: 10.1080/15592324.2019.1600394. Epub 2019 Apr 25.

Abstract

Scaffold protein Receptor for Activated C Kinase 1 (RACK1) is a negative regulator of plant stress hormone - abscisic acid (ABA) mediated pathways. RACK1 has been reported to regulate global miRNA biogenesis pathway in C. elegans, humans, and in Arabidopsis. RACK1 regulates different steps of miRNA biogenesis and stability in response to different stimuli in plants. miR393s is implicated in salt stress response pathway through an antagonistic response between the stress hormone ABA-mediated salt stress and growth hormone auxin. Specifically, the known auxin receptor clade transcripts TIR1/AFB2 are the target for the miR393s. By down-regulating the auxin signaling pathways, the miR393s inhibit the regulation of salt tolerance by auxin. Here we show that genetic loss of RACK1A- the predominant member of the three genes family of RACK1 in Arabidopsis, results in the inhibition of miR393 level causing the same salt sensitivities as the individual mir393a or mir393b or the double mutant mir393ab phenotypes. We propose that down-regulation of auxin signaling through RACK1A induced miR393 biogenesis potentially regulates the Arabidopsis acclimation to salinity. Our findings fill up a molecular gap in our understanding of the role of miR393 mediated ABA and auxin-regulated salt stress responses.

摘要

支架蛋白活化C激酶1受体(RACK1)是植物应激激素——脱落酸(ABA)介导途径的负调控因子。据报道,RACK1在秀丽隐杆线虫、人类和拟南芥中调节全局miRNA生物合成途径。RACK1在植物中响应不同刺激调节miRNA生物合成和稳定性的不同步骤。miR393s通过应激激素ABA介导的盐胁迫与生长激素生长素之间的拮抗反应参与盐胁迫响应途径。具体而言,已知的生长素受体进化枝转录本TIR1/AFB2是miR393s的靶标。通过下调生长素信号通路,miR393s抑制生长素对耐盐性的调节。在这里,我们表明,拟南芥中RACK1三个基因家族的主要成员RACK1A的基因缺失导致miR393水平受到抑制,从而导致与单个mir393a或mir393b或双突变体mir393ab表型相同的盐敏感性。我们提出,通过RACK1A诱导的miR393生物合成下调生长素信号通路,可能调节拟南芥对盐度的适应性。我们的发现填补了我们在理解miR393介导的ABA和生长素调节的盐胁迫反应作用方面的分子空白。

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