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Modeling quantitative interactions: the disease outcome of generalist fungal pathogen across the plant kingdom
  • +4
  • Celine Caseys,
  • Gongjun Shi,
  • Nicole Soltis,
  • Raoni Gwinner,
  • Jason Corwin,
  • Susanna Atwell,
  • Daniel Kliebenstein
Celine Caseys
University of California Davis
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Gongjun Shi
North Dakota State University
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Nicole Soltis
UC Davis
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Raoni Gwinner
Embrapa Amazonia ocidental, Manaus
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Jason Corwin
University of Colorado at Boulder
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Susanna Atwell
UC Davis
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Daniel Kliebenstein
UC Davis
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Abstract

Botrytis cinerea is a fungal pathogen that causes necrotic disease on more than a thousand known hosts widely spread across the plant kingdom. How B. cinerea interacts with such extensive host diversity remains largely unknown. To address this question, we generated an infectivity matrix of 98 strains of B. cinerea on 90 genotypes representing eight host plants. This experimental infectivity matrix revealed that the disease outcome is largely explained by variations in either the host resistance or pathogen virulence. However, the specific interactions between host and pathogen account for 16% of the disease outcome. Furthermore, the disease outcomes cluster among genotypes of a species but are independent of the relatedness between hosts. When analyzing the host specificity and virulence of B. cinerea, generalist strains are predominant. In this fungal necrotroph, specialization may happen by a loss in virulence on most hosts rather than an increase of virulence on a specific host. To uncover the genetic architecture of Botrytis, a genome-wide association study (GWAS) was performed and revealed 124 genes associated with host specificity and virulence. The genetic architecture of these traits is distinct, polygenic and widespread across B. cinerea genome. The complexity of the disease outcome is best explained by the additivity of small effect genes that adjust the infection to diverse hosts.