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Plant disease resistance

About: Plant disease resistance is a research topic. Over the lifetime, 12952 publications have been published within this topic receiving 381820 citations. The topic is also known as: plant innate immunity.


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Journal ArticleDOI
TL;DR: This review deals with the consistency of the genomic positions of quantitative trait loci (QTL) controlling resistance across different maize populations, and with the clustering of genes for resistance to S. turcica and other fungal pathogens or insect pests in the maize genome.
Abstract: Turcicum or northern corn leaf blight (NCLB) incited by the ascomycete Setosphaeria turcica, anamorph Exserohilum turcicum, is a ubiquitous foliar disease of maize. Diverse sources of qualitative and quantitative resistance are available but qualitative resistances (Ht genes) are often unstable. In the tropics especially, they are either overcome by new virulent races or they suffer from climatically sensitive expression. Quantitative resistance is expressed independently of the physical environment and has never succumbed to S. turcica pathotypes in the field. This review emphasizes the identification and mapping of genes related to quantitative NCLB resistance. We deal with the consistency of the genomic positions of quantitative trait loci (QTL) controlling resistance across different maize populations, and with the clustering of genes for resistance to S. turcica and other fungal pathogens or insect pests in the maize genome. Implications from these findings for further genomic research and resistance breeding are drawn. Incubation period (IP) and area under the disease progress curve (AUDPC), based on multiple disease ratings, are important component traits of quantitative NCLB resistance. They are generally tightly correlated (rp≅ 0.8) and highly heritable (h2≅ 0.75). QTL for resistance to NCLB (IP and AUDPC) were identified and characterized in three mapping populations (A, B, C). Population A, a set of 121-150 F3 families of the cross B52×mo17, represented US Corn Belt germplasm with a moderate level of resistance. It was field-tested in Iowa, USA, and Kenya, and genotyped at 112 restriction fragment length polymorphism (RFLP) loci. Population B consisted of 194-256 F3 families of the cross Lo951×CML202, the first parent being a Corn-Belt-derived European inbred line and the second parent being a highly resistant tropical African inbred line. The population was also tested in Kenya and genotyped with 110 RFLP markers. Population C was derived from a cross between two early-maturing European inbred lines, D32 and D145, both having a moderate level of resistance. A total of 220 F3 families were tested in Switzerland and characterized with 87 RFLP and seven SSR markers. In each of the three studies, 12-13 QTL were detected by composite interval mapping at a signifcance threshold of LOD=2.5. The phenotypic and the genotypic variance were explained to an extent of 50-70% and 60-80%, respectively. Gene action was additive to partly dominant, as in previous generation means and combining ability analyses with other genetic material. In each population, gene effects of the QTL were of similar magnitude and no putative major genes were discovered. QTL for AUDPC were located on chromosomes 1 to 9. All three populations carried QTL in identical genomic regions on chromosomes 3 (bin 3.06/07), 5 (bin 3.06/07) and 8 (bin 8.05/06). The major genes Ht2 and Htn1 were also mapped to bins 8.05 and 8.06, suggesting the presence of a cluster of closely linked major and minor genes. The chromosomal bins 3.05, 5.04 and 8.05, or adjacent intervals, were further associated with QTL and major genes for resistance to eight other fungal diseases and insect pests of maize. Bins 1.05/07 and 9.05 were found to carry population-specifc genes for resistance to S. turcica and other organisms. Several disease lesion mimic mutations, resistance gene analogues and genes encoding pathogenesis-related proteins were mapped to regions harbouring NCLB resistance QTL.

165 citations

Journal ArticleDOI
TL;DR: In this paper, the authors investigated whether RPW8.1 and R8.2 engage known pathway(s) for defence signalling, and they showed that EDR1, a gene encoding a conserved MAPKK kinase, exerts negative regulation on HR cell death and powdery mildew resistance by limiting the transcriptional amplification of R 8.2.
Abstract: Genetic studies have identified a number of components of signal transduction pathways leading to plant disease resistance and the accompanying hypersensitive response (HR) following detection of pathogens by plant resistance (R) genes. In Arabidopsis, the majority of R proteins so far characterized belong to a plant superfamily that have a central nucleotide-binding site and C-terminal leucine-rich-repeats (NB-LRRs). Another much less prevalent class comprises RPW8.1 and RPW8.2, two related proteins that possess a putative N-terminal transmembrane domain and a coiled-coil motif, and confer broad-spectrum resistance to powdery mildew. Here we investigated whether RPW8.1 and RPW8.2 engage known pathway(s) for defence signalling. We show that RPW8.1 and RPW8.2 recruit, in addition to salicylic acid and EDS1, the other NB-LRR gene-signalling components PAD4, EDS5, NPR1 and SGT1b for activation of powdery mildew resistance and HR. In contrast, NDR1, RAR1 and PBS3 that are required for function of certain NB-LRR R genes, and COI1 and EIN2 that operate, respectively, in the jasmonic acid and ethylene signalling pathways, do not contribute to RPW8.1 and RPW8.2-mediated resistance. We further demonstrate that EDR1, a gene encoding a conserved MAPKK kinase, exerts negative regulation on HR cell death and powdery mildew resistance by limiting the transcriptional amplification of RPW8.1 and RPW8.2. Our results suggest that RPW8.1 and RPW8.2 stimulate a conserved basal defence pathway that is negatively regulated by EDR1.

165 citations

Journal ArticleDOI
TL;DR: Gene pyramiding produced lines with high CBB resistance, and is thus, a suitable method for developing CBB-resistant cultivars of different market classes.
Abstract: Common bean (Phaseolus vulgaris L.) is highly susceptible to common bacterial blight (CBB), caused by Xanthomonas campestris pv. phaseoli (Smith) Dye. High levels of cultivar resistance would minimize yield losses, reduce bactericide use and production costs, and facilitate integrated disease-and-crop management and the production and distribution of pathogen-free seed. We aimed to (i) assess the levels of CBB resistance of different Phaseolus species in the tropics, (ii) determine the CBB reaction of resistant cultivars and advanced breeding lines, and (iii) report on CBB resistance of lines developed from P. vulgaris × P. acutifolius (tepary bean) hybridization and gene pyramiding at CIAT. Between 1994 and 1998, we evaluated, in the field, 162 accessions of tepary, scarlet runner (P. coccineus), lima (P. lunatus), and common beans, 119 CBB-resistant cultivars and advanced breeding lines of common bean, and six lines recently developed by interspecific hybridization and gene pyramiding. For inoculation, we used aspersion, surgical blades, and/or multiple needles. The highest levels (scores of 1.2-2.0) of CBB resistance were found in P. acutifolius accessions, G40029 and G40156, followed by P. lunatus (scores of 4.2-6.2), P. coccineus (scores of 4.8-5.5), and P. vulgaris (scores of 4.5-6.4). Resistance available in P. coccineus and P. vulgaris landraces has already been transferred to common bean. But resistance transferred from P. acutifolius was much lower (scores of 3.8-4.5) than those available. Gene pyramiding produced lines with high CBB resistance (scores of 1.5-2.4), and is thus, a suitable method for developing CBB-resistant cultivars of different market classes.

165 citations

Journal ArticleDOI
TL;DR: Heterologous expression of the fungal afp gene and the barley chitinase II gene in wheat demonstrated that colony formation and, thereby, spreading of two important biotrophic fungal diseases is inhibited.
Abstract: Three cDNAs encoding the antifungal protein Ag-AFP from the fungus Aspergillus giganteus, a barley class II chitinase and a barley type I RIP, all regulated by the constitutive Ubiquitin1 promoter from maize, were expressed in transgenic wheat. In 17 wheat lines, stable integration and inheritance of one of the three transgenes has been demonstrated over four generations. The formation of powdery mildew (Erysiphe graminis f. sp. tritici) or leaf rust (Puccinia recondita f. sp. tritici) colonies was significantly reduced on leaves from afp or chitinase II- but not from rip I-expressing wheat lines compared with nontransgenic controls. The increased resistance of afp and chitinase II lines was dependent on the dose of fungal spores used for inoculation. Heterologous expression of the fungal afp gene and the barley chitinase II gene in wheat demonstrated that colony formation and, thereby, spreading of two important biotrophic fungal diseases is inhibited approximately 40 to 50% at an inoculum density of 80 to 100 spores per cm 2 .

164 citations

Book ChapterDOI
TL;DR: The differences and similarities of defenses and defensive signaling directed against viral versus nonviral pathogens, the potential role of RNA silencing as an effector in resistance and possible regulator of defensive signaling are discussed.
Abstract: Induced mechanisms are by definition imperceptible or less active in uninfected, unstressed, or untreated plants, but can be activated by pathogen infection, stress, or chemical treatment to inhibit the replication and movement of virus in the host. In contrast, defenses that are pre-existing or serve to limit virus propagation and spread in otherwise susceptible hosts are considered to be "basal" in nature. Both forms of resistance can be genetically determined. Most recessive resistance genes that control resistance to viruses appear not to depend upon inducible mechanisms but rather maintain basal resistance by producing nonfunctional variants of factors, specifically translation initiation factors, required by the virus for successful exploitation of the host cell protein synthetic machinery. In contrast, most dominant resistance genes condition the induction of broad-scale changes in plant biochemistry and physiology that are activated and regulated by various signal transduction pathways, particularly those regulated by salicylic acid, jasmonic acid, and ethylene. These induced changes include localized plant cell death (associated with the hypersensitive response, HR) and the upregulation of resistance against many types of pathogen throughout the plant (systemic acquired resistance, SAR). Unfortunately, it is still poorly understood how virus infection is inhibited and restricted during the HR and in plants exhibiting SAR. Resistance to viruses is not always genetically predetermined and can be highly adaptive in nature. This is exemplified by resistance based on RNA silencing, which appears to play roles in both induced and basal resistance to viruses. To counter inducible resistance mechanisms, viruses have acquired counter-defense factors to subvert RNA silencing. Some of these factors may affect signal transduction pathways controlled by salicylic acid and jasmonic acid. In this chapter, we review current knowledge of defensive signaling in resistance to viruses including the nature and roles of low molecular weight, proteinaceous, and small RNA components of defensive signaling. We discuss the differences and similarities of defenses and defensive signaling directed against viral versus nonviral pathogens, the potential role of RNA silencing as an effector in resistance and possible regulator of defensive signaling, crosstalk and overlap between antiviral systems, and interference with and manipulation of host defensive systems by the viruses themselves.

164 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
2023377
2022756
2021410
2020438
2019526
2018640