Genome-Wide Association and Selective Sweep Studies Reveal the Complex Genetic Architecture of DMI Fungicide Resistance in <i>Cercospora beticola</i>

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dc.contributor.authorSpanner, Rebecca
dc.contributor.authorTaliadoros, Demetris
dc.contributor.authorRichards, Jonathan
dc.contributor.authorRivera-Varas, Viviana
dc.contributor.authorNeubauer, Jonathan
dc.contributor.authorNatwick, Mari
dc.contributor.authorHamilton, Olivia
dc.contributor.authorVaghefi, Niloofar
dc.contributor.authorPethybridge, Sarah
dc.contributor.authorSecor, Gary A.
dc.contributor.authorFriesen, Timothy L.
dc.contributor.authorStukenbrock, Eva H.
dc.contributor.authorBolton, Melvin D.
dc.date.accessioned2025-01-20T22:09:15Z
dc.date.available2025-01-20T22:09:15Z
dc.date.issued2021
dc.description.abstractThe rapid and widespread evolution of fungicide resistance remains a challenge for crop disease management. The demethylation inhibitor (DMI) class of fungicides is a widely used chemistry for managing disease, but there has been a gradual decline in efficacy in many crop pathosystems. Reliance on DMI fungicides has increased resistance in populations of the plant pathogenic fungus Cercospora beticola worldwide. To better understand the genetic and evolutionary basis for DMI resistance in C. beticola, a genome-wide association study (GWAS) and selective sweep analysis were conducted for the first time in this species. We performed whole-genome resequencing of 190 C. beticola isolates infecting sugar beet (Beta vulgaris ssp. volgaris). All isolates were phenotyped for sensitivity to the DMI tetraconazole. Intragenic markers on chromosomes 1, 4, and 9 were significantly associated with DMI fungicide resistance, including a polyketide synthase gene and the gene encoding the DMI target CbCYP51. Haplotype analysis of CbCYP51 identified a synonymous mutation (E170) and nonsynonymous mutations (L144F, 1387M, and Y4645) associated with DMI resistance. Genome-wide scans of selection showed that several of the GWAS mutations for fungicide resistance resided in regions that have recently undergone a selective sweep. Using radial plate growth on selected media as a fitness proxy, we did not find a trade-off associated with DMI fungicide resistance. Taken together, we show that population genomic data from a crop pathogen can allow the identification of mutations conferring fungicide resistance and inform about their origins in the pathogen population.
dc.fuente.origenWOS
dc.identifier.doi10.1093/gbe/evab209
dc.identifier.issn1759-6653
dc.identifier.urihttps://doi.org/10.1093/gbe/evab209
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/94326
dc.identifier.wosidWOS:000731090000022
dc.issue.numero9
dc.language.isoen
dc.revistaGenome biology and evolution
dc.rightsacceso restringido
dc.subjectGWAS
dc.subjectCYP51
dc.subjectazole
dc.subjectsynonymous mutation
dc.subjectanti-fungal
dc.subjectselection
dc.subject.ods13 Climate Action
dc.subject.ods02 Zero Hunger
dc.subject.odspa13 Acción por el clima
dc.subject.odspa02 Hambre cero
dc.titleGenome-Wide Association and Selective Sweep Studies Reveal the Complex Genetic Architecture of DMI Fungicide Resistance in <i>Cercospora beticola</i>
dc.typeartículo
dc.volumen13
sipa.indexWOS
sipa.trazabilidadWOS;2025-01-12
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