Defects in the ferroxidase that participates in the reductive iron assimilation system results in hypervirulence in botrytis cinerea

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dc.contributor.authorVasquez-Montaño, E.
dc.contributor.authorHoppe, G.
dc.contributor.authorVega, A.
dc.contributor.authorOlivares-Yañez, C.
dc.contributor.authorCanessa, P.
dc.date.accessioned2021-08-27T18:34:18Z
dc.date.available2021-08-27T18:34:18Z
dc.date.issued2020
dc.descriptionIndexación: Scopus.es
dc.description.abstractAbstract The plant pathogen Botrytis cinerea is responsible for gray-mold disease, which infects a wide variety of species. The outcome of this host-pathogen interac-tion, a result of the interplay between plant defense and fungal virulence pathways, can be modulated by various environmental factors. Among these, iron availability and acquisition play a crucial role in diverse biological functions. How B. cinerea ob-tains iron, an essential micronutrient, during infection is unknown. We set out to deter-mine the role of the reductive iron assimilation (RIA) system during B. cinerea infection. This system comprises the BcFET1 ferroxidase, which belongs to the multicopper oxidase (MCO) family of proteins, and the BcFTR1 membrane-bound iron permease. Gene knockout and complementation studies revealed that, compared to the wild type, the bcfet1 mutant displays delayed conidiation, iron-dependent sclerotium pro-duction, and significantly reduced whole-cell iron content. Remarkably, this mutant exhibited a hypervirulence phenotype, whereas the bcftr1 mutant presents normal virulence and unaffected whole-cell iron levels and developmental programs. Inter-estingly, while in iron-starved plants wild-type B. cinerea produced slightly reduced necrotic lesions, the hypervirulence phenotype of the bcfet1 mutant is no longer observed in iron-deprived plants. This suggests that B. cinerea bcfet1 knockout mutants require plant-derived iron to achieve larger necrotic lesions, whereas in planta analyses of reactive oxygen species (ROS) revealed increased ROS levels only for infections caused by the bcfet1 mutant. These results suggest that increased ROS produc-tion, under an iron sufficiency environment, at least partly underlie the observed infection phenotype in this mutant. IMPORTANCE The plant-pathogenic fungus B. cinerea causes enormous economic losses, estimated at anywhere between $10 billion and $100 billion worldwide, under both pre-and postharvest conditions. Here, we present the characterization of a loss-of-function mutant in a component involved in iron acquisition that displays hyperviru-lence. While in different microbial systems iron uptake mechanisms appear to be critical to achieve full pathogenic potential, we found that the absence of the ferroxidase that is part of the reductive iron assimilation system leads to hypervirulence in this fungus. This is an unusual and rather underrepresented phenotype, which can be modulated by iron levels in the plant and provides an unexpected link between iron acquisition, reactive oxygen species (ROS) production, and pathogenesis in the Botrytis-plant interaction.es
dc.description.urihttps://journals.asm.org/doi/epdf/10.1128/mBio.01379-20
dc.identifier.citationmBio, Volume 11, Issue 4, Pages 1 - 20, 2020, Article number e01379-20es
dc.identifier.doiDOI: 10.1128/mBio.01379-20
dc.identifier.issn2161-2129
dc.identifier.urihttp://repositorio.unab.cl/xmlui/handle/ria/20032
dc.language.isoenes
dc.publisherAmerican Society for Microbiologyes
dc.rights.licenseAttribution 4.0 International (CC BY 4.0)
dc.subjectBotrytis cinereaes
dc.subjectFerroxidasees
dc.subjectHypervirulencees
dc.subjectIron uptakees
dc.subjectMulticopper oxidaseses
dc.subjectReductive iron assimilationes
dc.titleDefects in the ferroxidase that participates in the reductive iron assimilation system results in hypervirulence in botrytis cinereaes
dc.typeArtículoes
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