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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: A powdery mildew resistance gene, originating from wild emmerwheat (Triticum dicoccoides) accession `C20', from Rosh Pinna, Israel, was successfully transferred to hexaploid wheat through crossing and backcrossing and is designated Pm30.
Abstract: Powdery mildew caused by Erysiphe graminis f. sp. tritici is one of the most important wheat diseases in many regions of theworld. A powdery mildew resistance gene, originating from wild emmerwheat (Triticum dicoccoides) accession `C20', from Rosh Pinna, Israel,was successfully transferred to hexaploid wheat through crossing andbackcrossing. Genetic analysis indicated that a single dominant genecontrols the powdery mildew resistance at the seedling stage. SegregatingBC1F2 progenies of the cross 87-1/C20//2*8866 wereused for bulked segregant analysis (BSA). The PCR approach was used togenerate polymorphic DNA fragments between the resistant and susceptibleDNA pools by use of 10-mer random primers, STS primers, and wheatmicrosatellite primers. Three markers, Xgwm159/430,Xgwm159/460, and Xgwm159/500, were found to be linked tothe resistance gene. After evaluating the polymorphic markers in twosegregating populations, the distance between the markers and the mildewresistance gene was estimated to be 5–6 cM. By means of ChineseSpring nullisomic-tetrasomics and ditelosomics, the polymorphic markersand the resistance gene were assigned to chromosome arm 5BS and werephysically mapped on the gene rich regions of fragment length (FL) 0.41–0.43 by Chinese Spring deletion lines. As no powdery mildew resistancegene has been reported on chromosome arm 5BS, the mildew resistancegene originating from C20 should be a new gene and is designated Pm30.

140 citations

Journal ArticleDOI
TL;DR: Results confirmed that physiological resistance as detected by the straw lest was an integral component of field resistance, and that both physiological and avoidance mechanisms contributed to field resistance in the A 55/G 122 population.
Abstract: Physiological resistance is an important component of integrated strategies used to control white mold [caused by Sclerotinia sclerotiorum (Lib.) de Bary] a major disease of common bean (Phaseolus volgaris L.) in North America. Information pertaining to inheritance of physiological resistance, as detected by the greenhouse straw test, and its relationship with field resistance is lacking. The objectives of this study were to compare physiological resistance as detected by two separate straw tests with field resistance, evaluate heritability of physiological resistance, and to characterize the disease reaction of G 122 by quantitative trait locus (QTL) analysis. This was done in a recombioant inbred population (A 55/G 122) consisting of 67 F derived lines. The greenhouse tests with five and six replications, respectively, and the field test with three replications were conducted in randomized complete block designs. Moderate heritability for disease reaction (scored from 1 = no symptoms to 9 = severe disease) was observed across the straw tests (0.65) and in the field (0.78). Inheritance of disease reaction was further investigated with a framework linkage map composed of 74 markers, Interval mapping detected a QTL on linkage group B7 near the phaseolin seed protein (Phs) locus that explained 38% of the phenotypic variation for disease score across the straw tests. The same B7 QTL (26%), and an additional QTL (18%) on B1 near the fin gene for determinate growth habit conditioned field resistance. A QTL (34%) for canopy porosity, a measure of potential disease avoidance, also mapped to the fin locus. Results confirmed that physiological resistance as detected by the straw lest was an integral component of field resistance, and that both physiological and avoidance mechanisms contributed to field resistance in the A 55/G 122 population. The landrace G 122 clearly provides breeders with a heritable source of physiological resistance to combat white mold discase.

139 citations

Journal ArticleDOI
TL;DR: It is suggested that pathogen-inducible production of ET in transgenic rice can enhance resistance to necrotrophic and hemibiotrophic fungal pathogens without negatively impacting crop productivity.
Abstract: Rice blast (Magnaporthe oryzae) and sheath blight (Rhizoctonia solani) are the two most devastating diseases of rice (Oryza sativa), and have severe impacts on crop yield and grain quality. Recent evidence suggests that ethylene (ET) may play a more prominent role than salicylic acid and jasmonic acid in mediating rice disease resistance. In this study, we attempt to genetically manipulate endogenous ET levels in rice for enhancing resistance to rice blast and sheath blight diseases. Transgenic lines with inducible production of ET were generated by expressing the rice ACS2 (1-aminocyclopropane-1-carboxylic acid synthase, a key enzyme of ET biosynthesis) transgene under control of a strong pathogen-inducible promoter. In comparison with the wild-type plant, the OsACS2-overexpression lines showed significantly increased levels of the OsACS2 transcripts, endogenous ET and defence gene expression, especially in response to pathogen infection. More importantly, the transgenic lines exhibited increased resistance to a field isolate of R. solani, as well as different races of M. oryzae. Assessment of the growth rate, generational time and seed production revealed little or no differences between wild type and transgenic lines. These results suggest that pathogen-inducible production of ET in transgenic rice can enhance resistance to necrotrophic and hemibiotrophic fungal pathogens without negatively impacting crop productivity.

139 citations

Journal ArticleDOI
TL;DR: To identify genetic loci associated with lodging resistance, plant height and reaction to mycosphaerella blight in pea, a population consisting of 88 recombinant inbred lines was developed from a cross between Carneval and MP1401.
Abstract: With the development of genetic maps and the identification of the most-likely positions of quantitative trait loci (QTLs) on these maps, molecular markers for lodging resistance can be identified. Consequently, marker-assisted selection (MAS) has the potential to improve the efficiency of selection for lodging resistance in a breeding program. This study was conducted to identify genetic loci associated with lodging resistance, plant height and reaction to mycosphaerella blight in pea. A population consisting of 88 recombinant inbred lines (RILs) was developed from a cross between Carneval and MP1401. The RILs were evaluated in 11 environments across the provinces of Manitoba, Saskatchewan and Alberta, Canada in 1998, 1999 and 2000. One hundred and ninety two amplified fragment length polymorphism (AFLP) markers, 13 random amplified polymorphic DNA (RAPD) markers and one sequence tagged site (STS) marker were assigned to ten linkage groups (LGs) that covered 1,274 centi Morgans (cM) of the pea genome. Six of these LGs were aligned with the previous pea map. Two QTLs were identified for lodging resistance that collectively explained 58% of the total phenotypic variation in the mean environment. Three QTLs were identified each for plant height and resistance to mycosphaerella blight, which accounted for 65% and 36% of the total phenotypic variation, respectively, in the mean environment. These QTLs were relatively consistent across environments. The AFLP marker that was associated with the major locus for lodging resistance was converted into the sequence-characterized amplified-region (SCAR) marker. The presence or absence of the SCAR marker corresponded well with the lodging reaction of 50 commercial pea varieties.

139 citations

Journal ArticleDOI
TL;DR: A novel role for a RanGAP in the function of a plant disease resistance response is demonstrated by co-immunoprecipitation that this interaction is mediated in planta through the putative signaling domain at the Rx amino terminus.
Abstract: Race-specific disease resistance in plants is mediated by the products of host disease resistance (R) genes. Plant genomes possess hundreds of R gene homologs encoding nucleotide-binding and leucine-rich repeat (NB-LRR) proteins. NB-LRR proteins induce a disease resistance response following recognition of pathogen-encoded avirulence (Avr) proteins. However, little is known about the general mechanisms by which NB-LRR proteins recognize Avr proteins or how they subsequently induce defense responses. The Rx NB-LRR protein of potato confers resistance to potato virus X (PVX). Using a co-purification strategy, we have identified a Ran GTPase-activating protein (RanGAP2) as an Rx-interacting protein. We show by co-immunoprecipitation that this interaction is mediated in planta through the putative signaling domain at the Rx amino terminus. Overexpression of RanGAP2 results in activation of certain Rx derivatives. Likewise, knocking down RanGAP2 expression in Nicotiana benthamiana by virus-induced gene silencing compromises Rx-mediated resistance to PVX. Thus, we have demonstrated a novel role for a RanGAP in the function of a plant disease resistance response.

139 citations


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