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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 model pathosystem to dissect genetically the disease resistance response of plants against phytopathogenic bacteria is presented and it is shown that at least parts of this system fit the paradigms of Flor's 'gene-for-gene' hypothesis.
Abstract: We present a model pathosystem to dissect genetically the disease resistance response of plants against phytopathogenic bacteria. The interaction between Pseudomonas syringae pathovar maculicola (Psm) and Arabidopsis thaliana displays phenotypic varia-ion which depends on the genotype of both partners. Compatible interactions are defined by sustained in-planta bacterial growth and are normally accompanied of their appearance. For compatible interactions, resistance is defined by limited in-planta bacterial growth accompanied by a typical 'hypersensitive response' (HR). We show that at least parts of this system fit the paradigms of Flor's 'gene-for-gene' hypothesis. We identify functionally a putative bacterial avirulence gene (avrRpm 1) from a Psm isolate which conditions the HR on A. thaliana ecotypes Oy-0 abd Col- 0, but not Nd-0. We also demonstrate that resistance to the Psm strain from which avrRpm1 was isolated segregates as a single trait in the crosses Col-o x Nd-0 and Nd-0 x Oy-0. Furthermore, we map this locus (RPM1) molecularly in the Col-0 x Nd-0 cross to a relatively small interval defined by two RFLP markers on A. thliana chromosome 3. Resistance in the second cross also maps to this locus and co-segregates with resistance to avrRpm1.

213 citations

Journal ArticleDOI
TL;DR: It is reported that the overexpression of Prf leads to enhanced resistance to a number of normally virulent bacterial and viral pathogens and leads to increased sensitivity to fenthion.
Abstract: Resistance in tomato to the bacterial pathogen Pseudomonas syringae pathovar tomato requires Pto and Prf. Mutations that eliminate Prf show a loss of both Pto resistance and sensitivity to the organophosphate insecticide fenthion, suggesting that Prf controls both phenotypes. Herein, we report that the overexpression of Prf leads to enhanced resistance to a number of normally virulent bacterial and viral pathogens and leads to increased sensitivity to fenthion. These plants express levels of salicylic acid comparable to plants induced for systemic acquired resistance (SAR) and constitutively express pathogenesis related genes. These results suggest that the overexpression of Prf activates the Pto and Fen pathways in a pathogen-independent manner and leads to the activation of SAR. Transgene-induced SAR has implications for the generation of broad spectrum disease resistance in agricultural crop plants.

212 citations

BookDOI
01 Jan 1995
TL;DR: The role and evolution of induced resistance in natural ecosystems, and its relationship to other types of plant defenses against disease are discussed in this paper, where Tuzun et al. discuss the application and implementation of induced systemic resistance.
Abstract: Induced resistance in Legumes B.J. Deverall, E.K. Dann. Induced resistance in the Solanaceae O.L. Ozeretkovskaya. Induced resistance in Cucurbits P. Hammerschmidt, P. Yang-Cashman. Induced resistance in Monocots U. Steiner, F. Schonbeck. Molecular regulation of systemic induced resistance B.A. Stermer. Thoughts on the role and evolution of induced resistance in natural ecosystems, and its relationship to other types of plant defenses against disease M.C. Heath. Practical application and implementation of induced resistance S. Tuzun, J. Kloepper. Induced systemic resistance -- An overview J. Kuc. Index.

211 citations

Journal ArticleDOI
TL;DR: The data suggest that activation of a single allele of susceptibility gene CsLOB1 by PthA4 is sufficient to induce citrus canker disease, and mutation in the promoters of both alleles of CslOB1 is probably required to generate canker-resistant plants.
Abstract: Citrus canker caused by Xanthomonas citri subspecies citri (Xcc) is a severe disease for most commercial citrus cultivars and responsible for significant economic losses worldwide. Generating canker-resistant citrus varieties will provide an efficient and sustainable solution to control citrus canker. Here, we report our progress in generating canker-resistant grapefruit by modifying the PthA4 effector binding elements (EBEs) in the CsLOB1 Promoter (EBEPthA4 -CsLOBP) of the CsLOB1 (Citrus sinensis Lateral Organ Boundaries) gene. CsLOB1 is a susceptibility gene for citrus canker and is induced by the pathogenicity factor PthA4, which binds to the EBEPthA4 -CsLOBP to induce CsLOB1 gene expression. There are two alleles, Type I and Type II, of CsLOB1 in Duncan grapefruit. Here, a binary vector was designed to disrupt the PthA4 EBEs in Type I CsLOB1 Promoter (TI CsLOBP) via epicotyl transformation of Duncan grapefruit. Four transgenic Duncan plants with targeted modification of EBEPthA4 -T1 CsLOBP were successfully created. As for Type I CsLOB1 promoter, the mutation rate was 15.63% (#D13), 14.29% (#D17), 54.54% (#D18) and 81.25% (#D22). In the presence of wild-type Xcc, transgenic Duncan grapefruit developed canker symptoms similarly as wild type. An artificially designed dTALE dCsLOB1.3, which specifically recognizes Type I CsLOBP, but not the mutated Type I CsLOBP or Type II CsLOBP, was developed to infect Duncan transformants. Consequently, #D18 had weakened canker symptoms and #D22 had no visible canker symptoms in the presence of XccΔpthA4:dCsLOB1.3. Our data suggest that activation of a single allele of susceptibility gene CsLOB1 by PthA4 is sufficient to induce citrus canker disease, and mutation in the promoters of both alleles of CsLOB1 is probably required to generate citrus canker-resistant plants. This work lays the groundwork to generate canker-resistant citrus varieties via Cas9/sgRNA in the future.

211 citations

Journal ArticleDOI
TL;DR: The use of markers linked to CMD2 for marker-assisted breeding of CMD resistance in Latin America and for increasing the cost-effectiveness of resistance breeding in Africa are discussed.
Abstract: Cassava mosaic disease (CMD) is the most-important disease of cassava (Manihot esculenta) in Africa, and is a potential threat to Latin American (LA) cassava production. Although this viral disease is still unknown in LA, its vector – the whitefly – has recently been found. The disease is best controlled through host-plant resistance, which was first found in third backcross derivatives of an interspecific cross between cassava and Manihot glaziovii, and is thought to be polygenic. Recently, high levels of resistance were also found in several Nigerian cassava landraces. Classical genetic analysis and molecular genetic-mapping of the landraces showed that a major dominant gene confers this resistance. Bulk segregant analysis (BSA) was used to quickly identify a simple sequence repeat (SSR) marker linked to the CMD-resistance gene. The marker, SSRY28, is located on linkage group R of the male-parent-derived molecular genetic map. The gene, designated as CMD2, is flanked by the SSR and RFLP marker GY1 at 9 and 8 cM, respectively. To our knowledge, this is the first report of qualitative virus resistance in cassava, and of molecular markers that tag CMD resistance in cassava. We discuss the use of markers linked to CMD2 for marker-assisted breeding of CMD resistance in Latin America and for increasing the cost-effectiveness of resistance breeding in Africa.

210 citations


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