Detoxification of cruciferous phytoalexins in Botrytis cinerea: Spontaneous dimerization of a camalexin metabolite

Pedras, M. Soledade C.; Hossain, S. M. Zakir; Snitynsky, Ryan B.

doi:10.1016/j.phytochem.2010.11.018

Cited by 49 publications

(41 citation statements)

References 25 publications

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“…These same defense compounds provide resistance to a number of other pathogens including nonhost microbes that each may also vary in their sensitivity to the compounds (Mithen et al, 1986(Mithen et al, , 1987Stotz et al, 2011;Zhang et al, 2015b;Bednarek and Osbourn, 2009;Clay et al, 2009). This generates a potential system whereby a plant has variation in defense compounds while a multitude of pathogens also have genetic variation in the ability to detoxify specific plant defense metabolites when investigated (Pedras and Khan, 1997;Ahiahonu, 2002, 2005;Pedras et al, 2011). This suggests that we need a new thesis that moves beyond the categorical classification of plant/pathogen interactions such that nonhost, host, and broad-spectrum resistance are intricately linked and simply revolve around the ability of a host to create a defense and a pathogen to counter that defense.…”

Section: Pathogen Genetics and Its Impact On Broad-spectrum Resistancementioning

confidence: 99%

Quantitative Resistance: More Than Just Perception of a Pathogen

2017

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ORCID IDs: 0000-0001-6455-8474 (J.A.C.); 0000-0001-5759-3175 (D.J.K.)Molecular plant pathology has focused on studying large-effect qualitative resistance loci that predominantly function in detecting pathogens and/or transmitting signals resulting from pathogen detection. By contrast, less is known about quantitative resistance loci, particularly the molecular mechanisms controlling variation in quantitative resistance. Recent studies have provided insight into these mechanisms, showing that genetic variation at hundreds of causal genes may underpin quantitative resistance. Loci controlling quantitative resistance contain some of the same causal genes that mediate qualitative resistance, but the predominant mechanisms of quantitative resistance extend beyond pathogen recognition. Indeed, most causal genes for quantitative resistance encode specific defense-related outputs such as strengthening of the cell wall or defense compound biosynthesis. Extending previous work on qualitative resistance to focus on the mechanisms of quantitative resistance, such as the link between perception of microbe-associated molecular patterns and growth, has shown that the mechanisms underlying these defense outputs are also highly polygenic. Studies that include genetic variation in the pathogen have begun to highlight a potential need to rethink how the field considers broad-spectrum resistance and how it is affected by genetic variation within pathogen species and between pathogen species. These studies are broadening our understanding of quantitative resistance and highlighting the potentially vast scale of the genetic basis of quantitative resistance.

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Section: Pathogen Genetics and Its Impact On Broad-spectrum Resistancementioning

confidence: 99%

Quantitative Resistance: More Than Just Perception of a Pathogen

2017

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“…Additionally, B. cinerea is a true haploid ascomycete that infects a wide range of evolutionarily distinct plant hosts, from bryophytes to eudicots. B. cinerea has elevated natural genetic variation that results in multiple major-effect polymorphisms in known virulence mechanisms, including the production of phytotoxic metabolites (Colmenares et al, 2002;Dalmais et al, 2011), enzymes that detoxify plant defense metabolites (Ferrari et al, 2003;Pedras et al, 2005Pedras et al, , 2007Pedras et al, , 2008Pedras et al, , 2009Pedras et al, , 2011Stefanato et al, 2009;Rowe et al, 2010), and the ability to degrade plant cell walls (Rowe and Kliebenstein, 2007;Schumacher et al, 2012Schumacher et al, , 2015Kumari et al, 2014). Because wild B. cinerea isolates have recombination and random mating, a population of isolates is a random intermixed sample of the diverse virulence mechanisms (Rowe and Kliebenstein, 2007;Kretschmer et al, 2009;Rowe et al, 2010;Kumari et al, 2014;Atwell et al, 2015;Corwin et al, 2016aCorwin et al, , 2016bZhang et al, 2016).…”

Section: Introductionmentioning

confidence: 99%

Plastic Transcriptomes Stabilize Immunity to Pathogen Diversity: The Jasmonic Acid and Salicylic Acid Networks within the Arabidopsis/Botrytis Pathosystem

et al. 2017

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To respond to pathogen attack, selection and associated evolution has led to the creation of plant immune system that are a highly effective and inducible defense system. Central to this system are the plant defense hormones jasmonic acid (JA) and salicylic acid (SA) and crosstalk between the two, which may play an important role in defense responses to specific pathogens or even genotypes. Here, we used the Arabidopsis thaliana-Botrytis cinerea pathosystem to test how the host's defense system functions against genetic variation in a pathogen. We measured defense-related phenotypes and transcriptomic responses in Arabidopsis wild-type Col-0 and JA-and SA-signaling mutants, coi1-1 and npr1-1, individually challenged with 96 diverse B. cinerea isolates. Those data showed genetic variation in the pathogen influences on all components within the plant defense system at the transcriptional level. We identified four gene coexpression networks and two vectors of defense variation triggered by genetic variation in B. cinerea. This showed that the JA and SA signaling pathways functioned to constrain/canalize the range of virulence in the pathogen population, but the underlying transcriptomic response was highly plastic. These data showed that plants utilize major defense hormone pathways to buffer disease resistance, but not the metabolic or transcriptional responses to genetic variation within a pathogen.

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“…That some necrotrophs, requiring non-living plant tissue as a nutrient source, can actually be facilitated by host detection and response is evidenced by a number of necrotrophic species that induce host PCD, including Botrytis cinerea and Sclerotinia sclerotiorum [7]–[9]. Other necrotrophs engage or evade plant defenses, for example by detoxification of plant defense products, such as phytoalexins [10], [11]. In many interactions with necrotrophs (and herbivores), the plant successfully defends itself via jasmonic acid (JA) and ethylene-dependent pathways [5], [6].…”

Section: Introductionmentioning

confidence: 99%

Evidence for a Common Toolbox Based on Necrotrophy in a Fungal Lineage Spanning Necrotrophs, Biotrophs, Endophytes, Host Generalists and Specialists

et al. 2012

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The Sclerotiniaceae (Ascomycotina, Leotiomycetes) is a relatively recently evolved lineage of necrotrophic host generalists, and necrotrophic or biotrophic host specialists, some latent or symptomless. We hypothesized that they inherited a basic toolbox of genes for plant symbiosis from their common ancestor. Maintenance and evolutionary diversification of symbiosis could require selection on toolbox genes or on timing and magnitude of gene expression. The genes studied were chosen because their products have been previously investigated as pathogenicity factors in the Sclerotiniaceae. They encode proteins associated with cell wall degradation: acid protease 1 (acp1), aspartyl protease (asps), and polygalacturonases (pg1, pg3, pg5, pg6), and the oxalic acid (OA) pathway: a zinc finger transcription factor (pac1), and oxaloacetate acetylhydrolase (oah), catalyst in OA production, essential for full symptom production in Sclerotinia sclerotiorum. Site-specific likelihood analyses provided evidence for purifying selection in all 8 pathogenicity-related genes. Consistent with an evolutionary arms race model, positive selection was detected in 5 of 8 genes. Only generalists produced large, proliferating disease lesions on excised Arabidopsis thaliana leaves and oxalic acid by 72 hours in vitro. In planta expression of oah was 10–300 times greater among the necrotrophic host generalists than necrotrophic and biotrophic host specialists; pac1 was not differentially expressed. Ability to amplify 6/8 pathogenicity related genes and produce oxalic acid in all genera are consistent with the common toolbox hypothesis for this gene sample. That our data did not distinguish biotrophs from necrotrophs is consistent with 1) a common toolbox based on necrotrophy and 2) the most conservative interpretation of the 3-locus housekeeping gene phylogeny – a baseline of necrotrophy from which forms of biotrophy emerged at least twice. Early oah overexpression likely expands the host range of necrotrophic generalists in the Sclerotiniaceae, while specialists and biotrophs deploy oah, or other as-yet-unknown toolbox genes, differently.

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Detoxification of cruciferous phytoalexins in Botrytis cinerea: Spontaneous dimerization of a camalexin metabolite

Cited by 49 publications

References 25 publications

Quantitative Resistance: More Than Just Perception of a Pathogen

Quantitative Resistance: More Than Just Perception of a Pathogen

Plastic Transcriptomes Stabilize Immunity to Pathogen Diversity: The Jasmonic Acid and Salicylic Acid Networks within the Arabidopsis/Botrytis Pathosystem

Evidence for a Common Toolbox Based on Necrotrophy in a Fungal Lineage Spanning Necrotrophs, Biotrophs, Endophytes, Host Generalists and Specialists

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