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Nature. 2019 Oct 9. doi: 10.1038/s41586-019-1637-x. [Epub ahead of print]

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

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Department of Biosciences, University of Exeter, Exeter, UK.
The Sainsbury Laboratory, University of East Anglia, Norwich, UK.
Gregor Mendel Institute of Molecular Plant Biology, Vienna, Austria.
School of Mathematical and Physical Sciences, Department of Mathematics, University of Sussex, Brighton, UK.
Department of Biosciences, University of Exeter, Exeter, UK.
The Sainsbury Laboratory, University of East Anglia, Norwich, UK.


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.


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