n nnnPlant basal resistance is activated by virulent pathogens insusceptible host plants. A Colletotrichum orbiculare fungalmutant defective in the SSD1 gene, which regulates cell wallcomposition, is restricted by host basal resistance responses.Here, we identified the Nicotiana benthamiana signaling pathwayinvolved in basal resistance by silencing the defense-relatedgenes required for restricting the growth of the C. orbicularemutant. Only silencing of MAP Kinase Kinase2 or of both SalicylicAcid Induced Protein Kinase (SIPK) and Wound Induced ProteinKinase (WIPK), two mitogen-activated protein (MAP) kinases,allowed the mutant to infect and produce necrotic lesions similarto those of the wild type on inoculated leaves. The fungal mutantpenetrated host cells to produce infection hyphae at a higherfrequency in SIPK WIPK-silenced plants than in nonsilenced plants,without inducing host cellular defense responses. Immunocomplexkinase assays revealed that SIPK and WIPK were more active inleaves inoculated with mutant fungus than with the wild type,suggesting that induced resistance correlates with MAP kinaseactivity. Infiltration of heat-inactivated mutant conidia inducedboth SIPK and WIPK more strongly than did those of the wildtype, while conidial exudates of the wild type did not suppressMAP kinase induction by mutant conidia. Therefore, activationof a specific MAP kinase pathway by fungal cell surface componentsdetermines the effective level of basal plant resistance.展开▼
机译:ABSTRACTn FONT> TH> TR> TABLE> n
n TOP n <字体颜色= 464c53>抽象 FONT> n 介绍 n 结果 n 讨论 n 方法 n 参考文献 n FONT> TH> TR> TABLE> n nnn植物的基础抗性被 SUP>感受态中的强力病原体激活可行的寄主植物。 SSD1 I>基因中的 Colletotrichum orbiculare i>真菌 SUP>突变缺陷型,可调节宿主细胞壁 SUP>的组成,受宿主基础限制 SUP>在这里,我们通过沉默与防御相关的 SUP>来识别与基础抗性有关的 Nicotiana benthamiana I>信号传导途径 SUP>。限制IC生长所需的基因。圆形 I> SUP>突变体。 MAP激酶激酶2 I>或水杨酸 SUP>酸诱导的蛋白激酶 I>( SIPK I>)和伤口仅沉默诱导蛋白 SUP>激酶 I>( WIPK I>),两个促分裂原活化蛋白(MAP)激酶 SUP>使突变体感染并产生坏死 SUP>类似于叶片上的野生型。 SIPK WIPK I>沉默的植物中,真菌突变体 SUP>穿透的宿主细胞以更高的 SUP>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 SUP>激酶分析表明,接种突变真菌的 SUP>叶中SIPK和WIPK的活性高于野生型, SUP>提示诱导抗性与MAP激酶 SUP>活性。热灭活的突变体分生孢子对SIPK和WIPK的 SUP>的浸润比野生 SUP>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 SUP>对特定MAP激酶途径的激活 SUP>决定了基础植物抗性的有效水平。 SUP>
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