Im Jong Hee, Cho Young-Hee, Kim Geun-Don, Kang Geun-Ho, Hong Jung-Woo, Yoo Sang-Dong
College of Life Sciences and Biotechnology, Korea University, Seoul, 136-713, South Korea.
Plant Cell Environ. 2014 Oct;37(10):2303-12. doi: 10.1111/pce.12375. Epub 2014 Jun 30.
Terrestrial plants are exposed to complex stresses of high salt-induced abscisic acid (ABA) and submergence-induced hypoxia when seawater floods fields. Many studies have investigated plant responses to individual stress conditions, but not so much for coupled or sequentially imposed stresses. We examined molecular regulatory mechanisms of gene expression underlying the cellular responses involved in crosstalk between salt and hypoxia stresses. Salt/ABA- and AtMYC2-dependent induction of a synthetic ABA-responsive element and the native RD22 promoters were utilized in our cell-based functional assays. Such promoter-based reporter induction was largely inhibited by hypoxia and hypoxia-inducible AKIN10 activity. Biochemical analyses showed that AKIN10 negatively modulates AtMYC2 protein accumulation via proteasome activity upon AKIN10 kinase activity-dependent protein modification. Further genetic analysis using transgenic plants expressing AKIN10 provided evidence that AKIN10 activity undermined AtMYC2-dependent salt tolerance. Our findings unravel a novel molecular interaction between the key signalling constituents leading crosstalk between salt and hypoxia stresses in Arabidopsis thaliana under the detrimental condition of submergence in saltwater.
当海水淹没农田时,陆生植物会面临由高盐诱导的脱落酸(ABA)和淹没诱导的缺氧等复杂胁迫。许多研究调查了植物对单一胁迫条件的反应,但对于联合或相继施加的胁迫研究较少。我们研究了盐胁迫和缺氧胁迫相互作用中细胞反应所涉及的基因表达的分子调控机制。在我们基于细胞的功能分析中,利用了盐/ABA和AtMYC2依赖的合成ABA反应元件和天然RD22启动子的诱导。这种基于启动子的报告基因诱导在很大程度上受到缺氧和缺氧诱导的AKIN10活性的抑制。生化分析表明,在依赖AKIN10激酶活性的蛋白质修饰后,AKIN10通过蛋白酶体活性负向调节AtMYC2蛋白的积累。使用表达AKIN10的转基因植物进行的进一步遗传分析提供了证据,表明AKIN10活性削弱了AtMYC2依赖的耐盐性。我们的研究结果揭示了在盐水淹没的不利条件下,拟南芥中导致盐胁迫和缺氧胁迫相互作用的关键信号成分之间的一种新的分子相互作用。