Belt Katharina, Huang Shaobai, Thatcher Louise F, Casarotto Hayley, Singh Karam B, Van Aken Olivier, Millar A Harvey
ARC Centre of Excellence in Plant Energy Biology, Faculty of Science, Bayliss Building M316, The University of Western Australia, 35 Stirling Highway, Crawley 6009, Western Australia, Australia (K.B., S.H., O.V.A., A.H.M.).
Commonwealth Scientific and Industrial Research Organisation (CSIRO), Agriculture and Food, Wembley, Washington 6913, Australia (L.F.T., H.C., K.B.S.); and.
Plant Physiol. 2017 Apr;173(4):2029-2040. doi: 10.1104/pp.16.00060. Epub 2017 Feb 16.
Mitochondria are known for their role in ATP production and generation of reactive oxygen species, but little is known about the mechanism of their early involvement in plant stress signaling. The role of mitochondrial succinate dehydrogenase (SDH) in salicylic acid (SA) signaling was analyzed using two mutants: (), which is a point mutation in SDH1 identified in a loss of SA signaling screen, and a knockdown mutant () for SDH assembly factor 2 that is required for FAD insertion into SDH1. Both mutants showed strongly decreased SA-inducible stress promoter responses and low SDH maximum capacity compared to wild type, while also showed low succinate affinity, low catalytic efficiency, and increased resistance to SDH competitive inhibitors. The SA-induced promoter responses could be partially rescued in , but not in , by supplementing the plant growth media with succinate. Kinetic characterization showed that low concentrations of either SA or ubiquinone binding site inhibitors increased SDH activity and induced mitochondrial HO production. Both and showed lower rates of SA-dependent HO production in vitro in line with their low SA-dependent stress signaling responses in vivo. This provides quantitative and kinetic evidence that SA acts at or near the ubiquinone binding site of SDH to stimulate activity and contributes to plant stress signaling by increased rates of mitochondrial HO production, leading to part of the SA-dependent transcriptional response in plant cells.
线粒体因其在ATP生成和活性氧产生中的作用而闻名，但对于其早期参与植物应激信号传导的机制却知之甚少。利用两个突变体分析了线粒体琥珀酸脱氢酶（SDH）在水杨酸（SA）信号传导中的作用：（），这是在SA信号缺失筛选中鉴定出的SDH1中的点突变体，以及SDH组装因子2的敲除突变体（），FAD插入SDH1需要该组装因子。与野生型相比，这两个突变体均显示SA诱导的应激启动子反应大幅降低，SDH最大容量较低，而（）还显示琥珀酸亲和力低、催化效率低以及对SDH竞争性抑制剂的抗性增加。通过在植物生长培养基中补充琥珀酸，SA诱导的启动子反应在（）中可部分恢复，但在（）中不能恢复。动力学表征表明，低浓度的SA或泛醌结合位点抑制剂均可增加SDH活性并诱导线粒体HO产生。（）和（）在体外均显示出较低的SA依赖性HO产生速率，这与其体内较低的SA依赖性应激信号反应一致。这提供了定量和动力学证据，表明SA作用于SDH的泛醌结合位点或其附近以刺激活性，并通过增加线粒体HO产生速率促进植物应激信号传导，从而导致植物细胞中部分SA依赖性转录反应。
