Cytoplasmic retention and degradation of a mitotic inducer enable plant infection by a pathogenic fungus
Abstract
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.
Data availability
All data generated or analysed during this study are included in the manuscript and supporting files. Source data files have been provided for Figures 1-8
Article and author information
Author details
Funding
Marie Curie ITN Grant (FUNGIBRAIN FP7-PEOPLE-2013-ITN-607963)
- Paola Bardetti
Marie Curie ITN Grant (ARIADNE PITN-GA-2009-237936)
- Sónia Marisa Castanheira
Deutsche Forschungsgemeinschaft
- Gerhard H Braus
Spanish Government (BIO2014-55398-R)
- José Pérez-Martín
Spanish Government (BIO2017-88938-R)
- José Pérez-Martín
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
Reviewing Editor
- Christian S Hardtke, University of Lausanne, Switzerland
Version history
- Received: May 31, 2019
- Accepted: October 16, 2019
- Accepted Manuscript published: October 17, 2019 (version 1)
- Version of Record published: December 2, 2019 (version 2)
Copyright
© 2019, Bardetti et al.
This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.
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