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Inverse modulation of the energy sensor Snf1-related protein kinase 1 on hypoxia adaptation and salt stress tolerance in Arabidopsis thaliana

机译:能量传感器Snf1相关蛋白激酶1对拟南芥低氧适应性和盐胁迫耐受性的反调节

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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
机译:当海水淹没田地时,陆生植物面临高盐诱导的脱落酸(ABA)和淹没引起的缺氧的复杂胁迫。许多研究已经调查了植物对单个胁迫条件的反应,但对于耦合胁迫或相继施加的胁迫,研究并不多。我们检查了涉及盐和缺氧应激之间的串扰的细胞反应的基因表达的分子调控机制。盐/ ABA和AtMYC2依赖性的合成ABA响应元件和天然RD22启动子的诱导被用于我们基于细胞的功能测定中。这种基于启动子的报告基因诱导在很大程度上被低氧和低氧诱导的AKIN10活性所抑制。生化分析表明,AKIN10在AKIN10激酶活性依赖性蛋白修饰后通过蛋白酶体活性对AtMYC2蛋白积聚产生负调控。使用表达AKIN10的转基因植物进行的进一步基因分析提供了AKIN10活性破坏了AtMYC2依赖性盐耐受性的证据。我们的发现揭示了在浸入水中的有害条件下,拟南芥中盐和缺氧胁迫之间的主要信号传导成分之间的新型分子相互作用,导致盐与缺氧胁迫之间的串扰

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