The Colletotrichum orbiculare ssd1 Mutant Enhances Nicotiana benthamiana Basal Resistance by Activating a Mitogen-Activated Protein Kinase Pathway
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The Colletotrichum orbiculare ssd1 Mutant Enhances Nicotiana benthamiana Basal Resistance by Activating a Mitogen-Activated Protein Kinase Pathway

机译:炭疽菌ssd1突变体通过激活丝裂原激活的蛋白激酶途径增强本氏烟草基础抗性。

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ABSTRACTnnn TOP
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nnnPlant basal resistance is activated by virulent pathogens in susceptible host plants. A Colletotrichum orbiculare fungal mutant defective in the SSD1 gene, which regulates cell wall composition, is restricted by host basal resistance responses. Here, we identified the Nicotiana benthamiana signaling pathway involved in basal resistance by silencing the defense-related genes required for restricting the growth of the C. orbiculare mutant. Only silencing of MAP Kinase Kinase2 or of both Salicylic Acid Induced Protein Kinase (SIPK) and Wound Induced Protein Kinase (WIPK), two mitogen-activated protein (MAP) kinases, allowed the mutant to infect and produce necrotic lesions similar to those of the wild type on inoculated leaves. The fungal mutant penetrated host cells to produce infection hyphae at a higher frequency in SIPK WIPK-silenced plants than in nonsilenced plants, without inducing host cellular defense responses. Immunocomplex kinase assays revealed that SIPK and WIPK were more active in leaves inoculated with mutant fungus than with the wild type, suggesting that induced resistance correlates with MAP kinase activity. Infiltration of heat-inactivated mutant conidia induced both SIPK and WIPK more strongly than did those of the wild type, while conidial exudates of the wild type did not suppress MAP kinase induction by mutant conidia. Therefore, activation of a specific MAP kinase pathway by fungal cell surface components determines the effective level of basal plant resistance.
机译:ABSTRACTn n n ”“ TOP
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nnn植物的基础抗性被 感受态中的强力病原体激活可行的寄主植物。 SSD1 基因中的 Colletotrichum orbiculare 真菌 突变缺陷型,可调节宿主细胞壁 的组成,受宿主基础限制 在这里,我们通过沉默与防御相关的 来识别与基础抗性有关的 Nicotiana benthamiana 信号传导途径 。限制IC生长所需的基因。圆形 突变体。 MAP激酶激酶2 水杨酸 酸诱导的蛋白激酶 SIPK )和伤口仅沉默诱导蛋白 激酶 WIPK ),两个促分裂原活化蛋白(MAP)激酶 使突变体感染并产生坏死 类似于叶片上的野生型。 SIPK WIPK 沉默的植物中,真菌突变体 穿透的宿主细胞以更高的 频率产生感染菌丝,而非沉默植物中的 < / SUP>而不会诱导宿主细胞防御反应。免疫复合物 激酶分析表明,接种突变真菌的 叶中SIPK和WIPK的活性高于野生型, 提示诱导抗性与MAP激酶 活性。热灭活的突变体分生孢子对SIPK和WIPK的 的浸润比野生 的浸润更强烈,而野生型的分生孢子渗出液却不能抑制 < / SUP>突变体分生孢子诱导的MAP激酶。因此,真菌细胞表面成分 对特定MAP激酶途径的激活 决定了基础植物抗性的有效水平。

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  • 来源
    《THE PLANT CELL》 |2009年第8期|2517-2526|共10页
  • 作者单位

    Laboratory of Plant Pathology, Graduate School of Life and Environmental Sciences, Kyoto Prefectural University, Kyoto 606-8522, Japan;

    Laboratory of Defense in Plant–Pathogen Interactions, Graduate School of Agriculture, Nagoya University, Aichi 464-8601, Japan;

    Laboratory of Defense in Plant–Pathogen Interactions, Graduate School of Agriculture, Nagoya University, Aichi 464-8601, Japan;

    Department of Plant–Microbe Interactions, Max Planck Institute for Plant Breeding Research, 50829 Koeln, Germany;

    Department of Plant–Microbe Interactions, Max Planck Institute for Plant Breeding Research, 50829 Koeln, Germany;

    Laboratory of Plant Pathology, Graduate School of Life and Environmental Sciences, Kyoto Prefectural University, Kyoto 606-8522, Japan;

    Laboratory of Plant Pathology, Graduate School of Life and Environmental Sciences, Kyoto Prefectural University, Kyoto 606-8522, Japan;

    Laboratory of Plant Pathology, Graduate School of Life and Environmental Sciences, Kyoto Prefectural University, Kyoto 606-8522, Japan;

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