Septin-Mediated Plant Cell Invasion by the Rice Blast Fungus, Magnaporthe oryzae

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Science  22 Jun 2012:
Vol. 336, Issue 6088, pp. 1590-1595
DOI: 10.1126/science.1222934

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Blasting Through

The fungus that causes rice blast disease, Magnaporthe oryzae, can lead to devastating reductions in rice yields. M. oryzae enters the plant by developing specialized infection structures called appressoria. Appressoria generate enormous internal turgor pressure that somehow creates invasive forces that physically break the plant cuticle. Dagdas et al. (p. 1590) found that a toroidal (doughnut-shaped) filamentous actin network forms at the base of the appressorium at the precise point where the penetration peg, which ruptures the rice leaf cuticle, will emerge. This network is scaffolded by means of four septin guanosine triphosphatases, which form a dynamic ring structure that colocalizes with F-actin. The findings reveal how fungi translate extreme pressure into localized physical force.


To cause rice blast disease, the fungus Magnaporthe oryzae develops a pressurized dome-shaped cell called an appressorium, which physically ruptures the leaf cuticle to gain entry to plant tissue. Here, we report that a toroidal F-actin network assembles in the appressorium by means of four septin guanosine triphosphatases, which polymerize into a dynamic, hetero-oligomeric ring. Septins scaffold F-actin, via the ezrin-radixin-moesin protein Tea1, and phosphatidylinositide interactions at the appressorium plasma membrane. The septin ring assembles in a Cdc42- and Chm1-dependent manner and forms a diffusion barrier to localize the inverse-bin-amphiphysin-RVS–domain protein Rvs167 and the Wiskott-Aldrich syndrome protein Las17 at the point of penetration. Septins thereby provide the cortical rigidity and membrane curvature necessary for protrusion of a rigid penetration peg to breach the leaf surface.

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