Shades of gray: the world of quantitative disease resistance

Poland, Jesse; Balint‐Kurti, Peter; Wisser, Randall J.; Pratt, Richard C.; Nelson, Rebecca

doi:10.1016/j.tplants.2008.10.006

Cited by 602 publications

(586 citation statements)

References 84 publications

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“…Since the QTL on chromosome 14 did not explain a large portion of the phenotypic variance, we did not expect to find differentially transcribed NBS-encoding genes, which tend to play a qualitative role in disease resistance, although this role is not absolute (Poland et al 2009). While a gene encoding FACT (FAcilitates Chromatin Transcription) complex subunit SSRP1 (Structure Specific Recognition Protein 1), which has a GO term associated with DNA binding, was differentially transcribed, we could not find any literature showing its role in disease resistance.…”

Section: Discussionmentioning

confidence: 94%

“…We used a susceptible V. vinifera genome sequence for our analysis as no resistant wild Vitis genome has been assembled, so our gene search was partially biased. We believe breeding with these quantitative genes will help to generate durably resistant grapevine cultivars compared to breeding solely with R genes (Poland et al 2009). Because we found that leaf trichomes have an effect on disease resistance in one F 1 family, breeding for leaf trichomes presents another opportunity to select for downy mildew disease resistance.…”

Section: Discussionmentioning

confidence: 99%

“…Resistance dependent on a single dominant locus is not seen as being durable, especially to an air-borne outcrossing pathogen like the one that causes grapevine downy mildew (Buonassisi et al 2017;McDonald and Linde 2002). By contrast, quantitative resistance is controlled by many genes, each of which contributes a small portion to the resistance phenotype (Poland et al 2009). Additionally, quantitative resistance can be controlled by different metabolic processes in the plant, including nucleotide-binding site leucine-rich repeat (NBS-LRR) resistance genes.…”

Section: Introductionmentioning

confidence: 99%

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Construction of a dense SNP map of a highly heterozygous diploid potato population and QTL analysis of tuber shape and eye depth

Prashar

Hornyik

Young³

et al. 2014

Theor Appl Genet

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Key message Downy mildew resistance across days post-inoculation, experiments, and years in two interspecific grapevine F 1 families was investigated using linear mixed models and Bayesian networks, and five new QTL were identified. Abstract Breeding grapevines for downy mildew disease resistance has traditionally relied on qualitative gene resistance, which can be overcome by pathogen evolution. Analyzing two interspecific F 1 families, both having ancestry derived from Vitis vinifera and wild North American Vitis species, across 2 years and multiple experiments, we found multiple loci associated with downy mildew sporulation and hypersensitive response in both families using a single phenotype model. The loci explained between 7 and 17% of the variance for either phenotype, suggesting a complex genetic architecture for these traits in the two families studied. For two loci, we used RNA-Seq to detect differentially transcribed genes and found that the candidate genes at these loci were likely not NBS-LRR genes. Additionally, using a multiple phenotype Bayesian network analysis, we found effects between the leaf trichome density, hypersensitive response, and sporulation phenotypes. Moderate-high heritabilities were found for all three phenotypes, suggesting that selection for downy mildew resistance is an achievable goal by breeding for either physical-or non-physical-based resistance mechanisms, with the combination of the two possibly providing durable resistance.

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Section: Discussionmentioning

confidence: 94%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Construction of a dense SNP map of a highly heterozygous diploid potato population and QTL analysis of tuber shape and eye depth

Prashar

Hornyik

Young³

et al. 2014

Theor Appl Genet

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“…This model predicts a coevolutionary process that would generate the observed amplification and polymorphism in genes encoding effectors in pathogens and PTI components and R proteins in plants. Determining general properties of these complex interaction systems, which also occur with many pathogenic fungi, oomycetes, and nematodes and their comparable effectors, has practical potential because of the widespread use of resistance breeding for crop protection and the frequent failure of resistance in the face of pathogen variation in the field (10).…”

mentioning

confidence: 99%

Genetic disassembly and combinatorial reassembly identify a minimal functional repertoire of type III effectors in Pseudomonas syringae

Cunnac

Chakravarthy

Kvitko

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

203

249

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The virulence of Pseudomonas syringae and many other proteobacterial pathogens is dependent on complex repertoires of effector proteins injected into host cells by type III secretion systems. The 28 well-expressed effector genes in the repertoire of the model pathogen P. syringae pv. tomato DC3000 were deleted to produce polymutant DC3000D28E. Growth of DC3000D28E in Nicotiana benthamiana was symptomless and 4 logs lower than that of DC3000ΔhopQ1-1, which causes disease in this model plant. DC3000D28E seemed functionally effectorless but otherwise WT in diagnostic phenotypes relevant to plant interactions (for example, ability to inject the AvrPto-Cya reporter into N. benthamiana). Various effector genes were integrated by homologous recombination into native loci or by a programmable or random in vivo assembly shuttle (PRIVAS) system into the exchangeable effector locus in the Hrp pathogenicity island of DC3000D28E. The latter method exploited dual adapters and recombination in yeast for efficient assembly of PCR products into programmed or random combinations of multiple effector genes. Native and PRIVAS-mediated integrations were combined to identify a minimal functional repertoire of eight effector genes that restored much of the virulence of DC3000ΔhopQ1-1 in N. benthamiana, revealing a hierarchy in effector function: AvrPtoB acts with priority in suppressing immunity, enabling other effectors to promote further growth (HopM1 and HopE1), chlorosis (HopG1), lesion formation (HopAM1-1), and near full growth and symptom production (AvrE, HopAA1-1, and/or HopN1 functioning synergistically with the previous effectors). DC3000D28E, the PRIVAS method, and minimal functional repertoires provide new resources for probing the plant immune system. effector-triggered immunity | pathogen-associated molecular pattern-triggered immunity | DNA shuffling | multigene recombineering | synthetic biology

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“…Plants may also carry receptors for pathogen recognition specificity domains that induce the expression of defensins, thionins, oxidative burst and other defence responses (Jones & Dangl 2006;Friedman & Baker 2007;Ting et al 2008) or evolve resistance (R) genes that enable qualitative resistance mechanisms that control a broad set of disease resistance responses capable of preventing pathogens from further growth. Poland et al (2009) suggested several hypotheses for a range of mechanisms underlying quantitative disease resistance (QDR) in maize that may utilise similar, but less dramatic, responses similar to those mediated by qualitative resistance factors, but conferring only partial and usually race non-specific response. Bluhm et al (2008) identified hydrolases and oxidoreductases in C. zeae-maydis type I responsible for cellulose degradation and cercosporin biosynthesis, respectively.…”

Section: Grey Leaf Spot Caused By Cercospora Zeae-maydismentioning

confidence: 99%

Infection process in resistant and susceptible maize (Zea mays L.) genotypes to Cercospora zeae-maydis (type II)

Lyimo¹,

Pratt²,

Mnyuku³

2013

Plant Prot. Sci.

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Lyimo H.J.F., Pratt R.C., Mnyuku R.S. O.W. (2013): Infection process in resistant and susceptible maize (Zea mays L.) genotypes to Cercospora zeae-maydis (type II). Plant Protect. Sci., 49: 11-18.The infection process of Cercospora zeae-maydis type II (syn. Cercospora zeina Meisel and Korsman) in resistant, moderately resistant and susceptible maize genotypes was studied in the greenhouse under artificial inoculation. The percent spore germination, germ tube growth and formation of mature appressorium on leaves at 24, 36, 48, and 72 h after inoculation did not differ between resistant, moderately resistant, and susceptible maize genotypes (P ≤ 0.05). More germlings were established after penetration on susceptible than resistant and moderately resistant maize genotypes at 72, 96, 120, and 144 h after inoculation. The hyphal wefts in cells of resistant and moderately resistant genotypes were shorter than in susceptible genotypes (P ≤ 0.05). The slow pathogen growth was associated with a reduced number of conidiophores per stroma, spores per unit area and smaller lesions. The reduced pathogen growth after penetration suggests possible involvement of pathogen growth inhibitory substances in maize resistance to C. zeae-maydis type II.

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Shades of gray: the world of quantitative disease resistance

Cited by 602 publications

References 84 publications

Construction of a dense SNP map of a highly heterozygous diploid potato population and QTL analysis of tuber shape and eye depth

Construction of a dense SNP map of a highly heterozygous diploid potato population and QTL analysis of tuber shape and eye depth

Genetic disassembly and combinatorial reassembly identify a minimal functional repertoire of type III effectors in Pseudomonas syringae

Infection process in resistant and susceptible maize (Zea mays L.) genotypes to Cercospora zeae-maydis (type II)

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