英国埃克塞特大学Nicholas J. Talbot小组研究发现，一种传感激酶控制由稻瘟菌引起的膨压驱动的植物感染。 这一研究成果2019年10月9日在线发表在《自然》上。

课题组人员发现，组氨酸激酶Sln1促使附着胞感受压力达到临界膨阈值，从而促进宿主渗透。研究人员发现Sln1传感器以压力依赖的方式定位于附着胞的孔，这与植物感染数学模型的预测相符。Δsln1突变体会产生过量的附着胞膨压，产生高度黑化、无功能的附着胞，并且不会组织叶片感染所需的隔膜和极性决定因素。Sln1与蛋白激酶C通路并行起作用，通过蛋白激酶A来调节cAMP依赖的信号通路。 Pkc1磷酸化NADPH氧化酶的调节分子NoxR。总的来说，这些信号通路调节附着胞膨压并触发生成入侵力量引起枯萎病。

研究人员表示，稻瘟病菌进入其寄主植物通过专门的增压感染细胞，称为附着胞，其物理性断裂叶角质层。膨压通过胞裂蛋白介导的细胞骨架重组，和肌动蛋白依赖的菌丝的突出来施加巨大的入侵力。然而，在附着胞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。

附：英文原文

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

Author: Lauren S. Ryder, Yasin F. Dagdas, Michael J. Kershaw, Chandrasekhar Venkataraman, Anotida Madzvamuse, Xia Yan, Neftaly Cruz-Mireles, Darren M. Soanes, Miriam Oses-Ruiz, Vanessa Styles, Jan Sklenar, Frank L. H. Menke, Nicholas J. Talbot

Issue&Volume: 2019-10-09

Abstract: 

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 cuticle1,2. Turgor is applied as an enormous invasive force by septin-mediated reorganization of the cytoskeleton and actin-dependent protrusion of a rigid penetration hypha3. 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 pressure-dependent manner, which is consistent with the predictions of a mathematical model for plant infection. A Δsln1 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.

DOI: 10.1038/s41586-019-1637-x

Source: https://www.nature.com/articles/s41586-019-1637-x