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Elife. 2019 Oct 17;8. pii: e48943. doi: 10.7554/eLife.48943.

Cytoplasmic retention and degradation of a mitotic inducer enable plant infection by a pathogenic fungus.

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Instituto de Biología Funcional y Genómica (CSIC), Salamanca, Spain.
Department of Molecular Microbiology and Genetics, Institute for Microbiology and Genetics, Georg-August-University, Göttingen, Germany.


In the fungus Ustilago maydis, sexual pheromones elicit mating resulting in an infective filament able to infect corn plants. Along this process a G2 cell cycle arrest is mandatory. Such as cell cycle arrest is initiated upon the pheromone recognition in each mating partner, and sustained once cell fusion occurred until the fungus enter the plant tissue. We describe that the initial cell cycle arrest resulted from inhibition of the nuclear transport of the mitotic inducer Cdc25 by targeting its importin, Kap123. Near cell fusion to take place, the increase on pheromone signaling promotes Cdc25 degradation, which seems to be important to ensure the maintenance of the G2 cell cycle arrest to lead the formation of the infective filament. This way, premating cell cycle arrest is linked to the subsequent steps required for establishment of the infection. Disabling this connection resulted in the inability of fungal cells to infect plants.


Ustilago maydis; cell cycle arrest; developmental biology; fungal development; infectious disease; microbiology; pheromone signalling; virulence

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