Quantitative disease resistance: Multifaceted players in plant defense

Gou, Mingyue; Balint‐Kurti, Peter; Xu, Mingliang; Yang, Qin

doi:10.1111/jipb.13419

Cited by 26 publications

(21 citation statements)

References 177 publications

(209 reference statements)

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“…Quantitative disease resistance (QDR) is another form of plant immunity that limits the damage caused by pathogen infection which is nearly universal, often durable and broad-spectrum (Roux et al ., 2014; Corwin and Kliebenstein, 2017). QDR requires genes from very diverse families, each having a small effect on resistance (Gou et al ., 2023), which makes the identification and characterization of QDR genes difficult. Interestingly, QDR is the only form of plant immunity that reduces disease symptoms caused by many organisms that actively kill host cells for infection, such as the necrotrophic pathogen Sclerotinia sclerotiorum (Niks et al ., 2015; Wang et al ., 2019).…”

Section: Introductionmentioning

confidence: 99%

Neutral transcriptome rewiring promotes QDR evolvability at the species level

Delplace,

Khafif,

Stam

et al. 2024

Preprint

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Quantitative disease resistance (QDR) is an immune response limiting the damage caused by pathogen infection in plants. It involves the transcriptomic reprogramming of numerous genes each having a weak contribution to the plant immunity phenotype. Despite QDR widespread and broad-spectrum nature, the evolution of the underlying transcriptome reprogramming remains largely uncharacterized. Here, we analyzed global gene expression in response to the necrotrophic fungusSclerotinia sclerotiorumin 23Arabidopsis thalianaaccessions of diverse origin and contrasted QDR phenotype. Over a half of the species pan-transcriptome displayed local responses toS. sclerotiorum, with global reprogramming patterns incongruent with accessions phylogeny. Due to frequent small-amplitude variations, only ~11% responsive genes were common to all accessions. They formed protein-protein interactions networks densely connecting both old and recent genes. Clustering of accessions based on global regulation patterns identified four subsets unrelated to QDR phenotypes, highlighting at least four distinct paths towards regulatory evolution of QDR at the species level. We identified WRKY and MYB-related DNA binding sites enriched in the 5′-regulatory regions of core and subset-specific responsive genes respectively. Our findings show that the evolution of QDR involves distinct gene reprogramming trajectories at the species level, associated with contrasted patterns of cis-regulatory variation.

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Section: Introductionmentioning

confidence: 99%

Neutral transcriptome rewiring promotes QDR evolvability at the species level

Delplace,

Khafif,

Stam

et al. 2024

Preprint

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“…In contrast, quantitative HPIs are non-specific and usually controlled by many genes of small but additive effect distributed across plant and pathogen genomes 13,14 . Due to the involvement of polygenic mutations in the evolutionary responses of both plants and pathogens 14 and reduced intraspecific competition among pathogen isolates co-occurring on the same plant [15][16][17] , quantitative HPIs are expected to require longer times for evolutionary change, thus contributing to increased durability of quantitative resistance in many crop plants and reduced evolution of their associated pathogens as documented in some systems 13 . However, evolutionary theory also suggests that QPR may select for a general increase in pathogen aggressiveness 12 , defined as the amount of disease caused by a pathogen strain 18 .…”

Section: Introductionmentioning

confidence: 99%

Quantitative plant resistance enhances pathogen adaptation to ecological stresses

Zhan,

Yang

et al. 2024

Preprint

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Host-pathogen interactions play an important role in shaping ecosystems with many fundamental and applied implications. However, many aspects of the processes, consequences and mechanisms of these antagonistic interactions are still unknown. Evolutionary theory hypothesizes that quantitative plant resistance (QPR) enhances pathogen pathogenicity, therefore, threatening ecological function and sustainability but this hypothesis has rarely been tested empirically. Here, we present results from an eco-evolutionary study of a quantitative plant-pathogen interaction using 16 potato varieties and >2000 Phytophthora infestans strains. Twelve functional traits in the P. infestans populations derived from the varieties were compared. Our results indicate that QPR enhances pathogen pathogenicity and facilitates pathogen adaptation to other disease management attempts including the development of qualitative plant resistance and fungicides, and to environmental and chemical stresses including salinity, UV radiation, H2O2, heat and cold. QPR also increases pathogen spore production and potential of sexual recombination thereby enhancing the generation of new variation for adaptation. Genome-wide analyses indicate that the observed patterns of functional variation result from escalated selection from potato with higher QPR and that a substantial of genome are involved in the adaptation genetically and epigenetically. Our results highlight a potential risk to ecological function and resilience associated with continuing deployment of QPR, particularly under future climate conditions and are expected to stimulate further investigation into this important phenomenon with many host-pathogen systems.

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“…As with the evolution of fungicide resistance, pathogens can evolve to overcome host resistance through selection for virulent strains. How quickly pathogens evolve virulence to resistant cultivars is strongly influenced by the genetic architecture of the resistance – single major resistance (R) genes with large effect are usually less durable compared to quantitative resistance encoded by many genes (Cowger and Brown, 2019; Gou et al, 2023). The evolution of virulence is also influenced by the amount of genetic diversity in the selected pathogen population, the deployment strategies used for the resistance genes, and the distribution of virulent pathogen genotypes across a heterogenous host population (Milgroom and Peever, 2003; Rimbaud et al, 2018; Stam and McDonald, 2018).…”

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Molecular epidemiology of Cercospora leaf spot on resistant and susceptible sugar beet hybrids

Chen,

Keunecke,

Neu

et al. 2023

Preprint

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Cercospora leaf spot (CLS), caused byCercospora beticola, is a major foliar disease impacting sugar beet production worldwide. The development of new resistant sugar beet hybrids provides a powerful tool to better manage the disease, but it is unclear how these hybrids affect CLS epidemiology. We used a molecular epidemiology approach to dissect natural epidemics of CLS affecting two susceptible and two resistant sugar beet hybrids with different levels of resistance at two field sites. Infected plants were geotagged on a weekly basis. Isolations ofC. beticolawere made from infected leaves and genotyped using six simple sequence repeat loci to identify clones. We determined that CLS epidemics had a later onset in plots planted to resistant hybrids, but once the pathogen established an infection, there was little difference between resistant and susceptible hybrids in the probability of localized spread and dispersal. We found that different clones often infected the same leaf and that clusters of infected plants were often colonized by a mixture of clones. There was little overall difference in genetic diversity between resistant and susceptible hybrids, however genotypic evenness differed at one site. In this site we found one genotype restricted to the resistant cultivars at a high frequency. We established that infections were not randomly distributed across the fields and we found that a single clone could spread over a distance of 100 m during a growing season.

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Quantitative disease resistance: Multifaceted players in plant defense

Cited by 26 publications

References 177 publications

Neutral transcriptome rewiring promotes QDR evolvability at the species level

Neutral transcriptome rewiring promotes QDR evolvability at the species level

Quantitative plant resistance enhances pathogen adaptation to ecological stresses

Molecular epidemiology of Cercospora leaf spot on resistant and susceptible sugar beet hybrids

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