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Quantitative interactions drive Botrytis cinerea disease outcome across the plant kingdom

View ORCID ProfileCeline Caseys, Gongjun Shi, View ORCID ProfileNicole Soltis, Raoni Gwinner, View ORCID ProfileJason Corwin, Susanna Atwell, View ORCID ProfileDaniel Kliebenstein
doi: https://doi.org/10.1101/507491
Celine Caseys
1Department of Plant Sciences, University of California, Davis, One Shields Avenue, Davis, CA, 95616, USA
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Gongjun Shi
1Department of Plant Sciences, University of California, Davis, One Shields Avenue, Davis, CA, 95616, USA
2Department of Plant Pathology, North Dakota State University, Fargo, ND, 58102, USA
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Nicole Soltis
1Department of Plant Sciences, University of California, Davis, One Shields Avenue, Davis, CA, 95616, USA
3Plant Biology Graduate Group, University of California, Davis, One Shields Avenue, Davis, CA 95616 USA
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Raoni Gwinner
1Department of Plant Sciences, University of California, Davis, One Shields Avenue, Davis, CA, 95616, USA
4Department of Agriculture, Universidade Federal de Lavras, Lavras - MG, 37200-000, Brazil
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Jason Corwin
1Department of Plant Sciences, University of California, Davis, One Shields Avenue, Davis, CA, 95616, USA
5Department of Ecology and Evolution Biology, University of Colorado, 1900 Pleasesant Street, 334 UCB, Boulder, CO, 80309-0334, USA
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Susanna Atwell
1Department of Plant Sciences, University of California, Davis, One Shields Avenue, Davis, CA, 95616, USA
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Daniel Kliebenstein
1Department of Plant Sciences, University of California, Davis, One Shields Avenue, Davis, CA, 95616, USA
6DynaMo Center of Excellence, University of Copenhagen, Thorvaldsensvej 40, DK-1871, Frederiksberg C, Denmark
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  • For correspondence: Kliebenstein@ucdavis.edu
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Abstract

Botrytis cinerea is a polyphagous fungal pathogen that causes necrotic disease on more than a thousand known hosts widely spread across the plant kingdom. While it is known that quantitative resistance in the host and quantitative virulence in the pathogen largely mediate this pathosystem, how this pathogen interacts with the extensive host diversity is unknown. Does this pathogen have quantitative virulence efficiency on all hosts or individual solutions for each host? To address this question, we generated an infectivity matrix of 98 strains of Botrytis cinerea on 90 genotypes representing eight host plants. This experimental infectivity matrix showed that the predominant sources of quantitative variation are between host species and among pathogen strains. Furthermore, the eight eudicot hosts interacted individually with Botrytis cinerea strains independently of the evolutionary relatedness between hosts. An additive quantitative model can explain the complexity of these interactions in which Botrytis host specificity and general virulence have distinct polygenic architectures.

Footnotes

  • The focus of the paper was changed after concern in peer-review about the experiment design for the analysis of co-evolution dynamics. This shifts the manuscript from looking specifically at co-evolution to trying to lay out the groundwork for how genetic variation in the host and pathogen are shaping the interaction across a number of eudicot lineages. We also address reviewer comments on host specificity and deepened the GWAS analysis.

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The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-NC 4.0 International license.
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Posted February 06, 2020.
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Quantitative interactions drive Botrytis cinerea disease outcome across the plant kingdom
Celine Caseys, Gongjun Shi, Nicole Soltis, Raoni Gwinner, Jason Corwin, Susanna Atwell, Daniel Kliebenstein
bioRxiv 507491; doi: https://doi.org/10.1101/507491
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Quantitative interactions drive Botrytis cinerea disease outcome across the plant kingdom
Celine Caseys, Gongjun Shi, Nicole Soltis, Raoni Gwinner, Jason Corwin, Susanna Atwell, Daniel Kliebenstein
bioRxiv 507491; doi: https://doi.org/10.1101/507491

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