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A sensor kinase controls turgor-driven plant infection by the rice blast fungus

机译：传感器激酶通过稻瘟病菌控制膨大驱动的植物感染

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The blast fungus Magnaporthe oryzae gains entry to its host plant by means of a specialized pressure-generating infection cell called an appressorium, which physically ruptures the leaf cuticle(1,2). Turgor is applied as an enormous invasive force by septin-mediated reorganization of the cytoskeleton and actin-dependent protrusion of a rigid penetration hypha(3). However, the molecular mechanisms that regulate the generation of turgor pressure during appressorium-mediated infection of plants remain poorly understood. Here we show that a turgor-sensing histidine-aspartate kinase, Sln1, enables the appressorium to sense when a critical turgor threshold has been reached and thereby facilitates host penetration. We found that the Sln1 sensor localizes to the appressorium pore in a pressuredependent manner, which is consistent with the predictions of a mathematical model for plant infection. A Delta sln1 mutant generates excess intracellular appressorium turgor, produces hyper-melanized non-functional appressoria and does not organize the septins and polarity determinants that are required for leaf infection. Sln1 acts in parallel with the protein kinase C cell-integrity pathway as a regulator of cAMP-dependent signalling by protein kinase A. Pkc1 phosphorylates the NADPH oxidase regulator NoxR and, collectively, these signalling pathways modulate appressorium turgor and trigger the generation of invasive force to cause blast disease.
机译：稻瘟病菌稻瘟病菌（Magnaporthe oryzae）通过一种专门的产生压力的感染细胞进入进入宿主植物，该感染细胞称为Appressorium，它会物理破裂叶片的表皮（1,2）。 Turgor通过Septin介导的细胞骨架重组和刚性渗透菌丝的肌动蛋白依赖性突起而被用作巨大的侵袭力（3）。然而，在appressorium介导的植物感染过程中调节膨大压力产生的分子机制仍然知之甚少。在这里，我们显示了一种能够感应膨胀的组氨酸-天冬氨酸激酶Sln1，能够使Appressorium感测何时达到临界膨胀阈值，从而促进宿主的渗透。我们发现Sln1传感器以压力依赖的方式定位于食欲孔，这与植物感染数学模型的预测相符。 Delta sln1突变体会产生过量的细胞内表皮膨胀，产生过度变黑的无功能表皮，并且不会组织叶片感染所需的隔膜和极性决定簇。 Sln1与蛋白激酶C细胞完整性途径并行发挥作用，通过蛋白激酶A调节cAMP依赖性信号传导。Pkc1使NADPH氧化酶调节剂NoxR磷酸化，这些信号传导途径共同调节食欲旺盛并触发侵袭力的产生。引起爆炸病。

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