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

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 and Nicholas J. Talbot ()
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Lauren S. Ryder: University of Exeter
Yasin F. Dagdas: University of Exeter
Michael J. Kershaw: University of Exeter
Chandrasekhar Venkataraman: University of Sussex
Anotida Madzvamuse: University of Sussex
Xia Yan: University of Exeter
Neftaly Cruz-Mireles: University of East Anglia
Darren M. Soanes: University of Exeter
Miriam Oses-Ruiz: University of Exeter
Vanessa Styles: University of Sussex
Jan Sklenar: University of East Anglia
Frank L. H. Menke: University of East Anglia
Nicholas J. Talbot: University of Exeter

Nature, 2019, vol. 574, issue 7778, 423-427

Abstract: 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.

Date: 2019
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DOI: 10.1038/s41586-019-1637-x

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