Quantitative interactions: the disease outcome of Botrytis cinerea across the plant kingdom

Author:

Caseys Celine1ORCID,Shi Gongjun12,Soltis Nicole13,Gwinner Raoni14ORCID,Corwin Jason15,Atwell Susanna1,Kliebenstein Daniel J16

Affiliation:

1. Department of Plant Sciences, University of California, Davis, Davis, CA 95616, USA

2. Department of Plant Pathology, North Dakota State University, Fargo, ND 58102, USA

3. Plant Biology Graduate Group, University of California, Davis, Davis, CA 95616 USA

4. Embrapa Amazonia Ocidental, Manaus 69010-970, Brazil

5. Department of Ecology and Evolution Biology, University of Colorado, Boulder, CO 80309-0334, USA

6. DynaMo Center of Excellence, University of Copenhagen, Frederiksberg C DK-1871, Denmark

Abstract

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 host specificity and virulence, a genome-wide association study (GWAS) was performed and revealed up to 1492 genes of interest. The genetic architecture of these traits is widespread across the B. cinerea genome. The complexity of the disease outcome might be explained by hundreds of functionally diverse genes putatively involved in adjusting the infection to diverse hosts.

Funder

National science foundation

Publisher

Oxford University Press (OUP)

Subject

Genetics (clinical),Genetics,Molecular Biology

Reference88 articles.

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