Liu Peiqing, Li Benjin, Lin Ming, Chen Guoliang, Ding Xueling, Weng Qiyong, Chen Qinghe
Institute of Plant Protection, Fujian Academy of Agricultural Sciences, Fuzhou, 350 003, China.
Fujian-Taiwan Joint Innovative Centre for Ecological Control of Crop Pests, Fujian Agriculture and Forestry University, Fuzhou 350 002, China.
Funct Plant Biol. 2016 Jun;43(6):563-574. doi: 10.1071/FP16006.
Phytophthora capsici is an oomycete pathogen with a broad host range that inflicts significant damage in vegetables. Phosphite (Phi) is used to control oomycete diseases, but the molecular mechanisms underlying Phi-induced resistance to P. capsici are unknown. Thus, Phi-inhibited mycelial growth on strain LT1534 and primed host defence were analysed. We demonstrated that Phi (>5µgmL-1) had a direct antibiotic effect on mycelial growth and zoospore production, and that mortality and DNA content were significantly reduced by pre-treatment with Phi. In addition, elevated hydrogen peroxide (H2O2) promoted callose deposition and increased the levels of soluble proteins and Capsicum annuum L. pathogenesis-related 1 (CaPR1) expression. Furthermore, Phi (1gL-1) significantly increased the transcription of the antioxidant enzyme genes, and the genes involved in ethylene (ET) and abscisic acid (ABA) biosynthesis, as well as mitogen-activated protein kinase (MAPK) cascades. However, pre-treatment with reactive oxygen species (ROS), ABA and ET biosynthesis inhibitors decreased Phi-induced resistance and reduced the expression of ABA-responsive 1 (CaABR1) and lipoxygenase 1 (CaLOX1). In addition, the decreased ROS and ABA inhibited Phi-induced expression of CaMPK17-1. We propose that Phi-induced ROS production, ET and ABA biosynthesis mediate the control of P. capsici, and that ABA functions through CaMPK17-1-mediated MAPK signalling.
辣椒疫霉是一种宿主范围广泛的卵菌病原体，对蔬菜造成重大损害。亚磷酸盐（Phi）用于控制卵菌病害，但Phi诱导对辣椒疫霉抗性的分子机制尚不清楚。因此，分析了Phi对LT1534菌株菌丝生长的抑制作用以及对宿主防御的引发作用。我们证明，Phi（>5µg/mL）对菌丝生长和游动孢子产生具有直接抗菌作用，并且Phi预处理可显著降低死亡率和DNA含量。此外，过氧化氢（H2O2）水平升高促进了胼胝质沉积，并增加了可溶性蛋白质水平和辣椒病程相关蛋白1（CaPR1）的表达。此外，Phi（1g/L）显著增加了抗氧化酶基因以及参与乙烯（ET）和脱落酸（ABA）生物合成的基因以及丝裂原活化蛋白激酶（MAPK）级联反应的转录。然而，用活性氧（ROS）、ABA和ET生物合成抑制剂预处理会降低Phi诱导的抗性，并降低ABA响应蛋白1（CaABR1）和脂氧合酶1（CaLOX1）的表达。此外，ROS和ABA的减少抑制了Phi诱导的CaMPK17-1表达。我们认为，Phi诱导的ROS产生、ET和ABA生物合成介导了对辣椒疫霉的控制，并且ABA通过CaMPK17-1介导的MAPK信号传导发挥作用。
