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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: Double mutant analysis of Atrar1 in combination with the R signal intermediate ndr1 suggests that AtRAR1 and NDR1 can operate in both linear and parallel signaling events, depending on the R gene function triggered.
Abstract: Plant disease resistance (R) genes mediate specific pathogen recognition, leading to a successful immune response. Downstream responses include ion fluxes, an oxidative burst, transcriptional reprogramming, and, in many cases, hypersensitive cell death at the infection site. We used a transgenic Arabidopsis line carrying the bacterial avirulence gene avrRpm1 under the control of a steroid-inducible promoter to select for mutations in genes required for RPM1-mediated recognition and signal transduction. We identified an allelic series of eight mutants that also were allelic to the previously identified pbs2 mutation. Positional cloning revealed this gene to be AtRAR1, the Arabidopsis ortholog of barley RAR1, a known mediator of R function. AtRAR1 is required for both full hypersensitive cell death and complete disease resistance mediated by many, but not all, tested R genes. Double mutant analysis of Atrar1 in combination with the R signal intermediate ndr1 suggests that AtRAR1 and NDR1 can operate in both linear and parallel signaling events, depending on the R gene function triggered. In Atrar1 null plants, the levels of RPM1-myc are reduced severely, suggesting that AtRAR1 may regulate R protein stability or accumulation.

253 citations

Journal ArticleDOI
TL;DR: It is demonstrated that cold stimulates proteolytic activation of a plasma membrane-tethered NAC (NAM/ATAF1/2/CUC2) transcription factor NTL6, which serves as a molecular link that incorporates cold signals into pathogen resistance responses.
Abstract: Cold signals interact with other environmental cues to modulate plant developmental processes. Recent studies have shown that many Pathogenesis-Related (PR) genes are induced and disease resistance is enhanced after exposure to low temperatures, linking cold signals with pathogenesis in plants. However, the underlying molecular mechanisms and signaling schemes are largely unknown. Here, we demonstrate that cold stimulates proteolytic activation of a plasma membrane-tethered NAC (NAM/ATAF1/2/CUC2) transcription factor NTL6. The transcriptionally active NTL6 protein enters the nucleus, where it induces a subset of PR genes by directly binding to a conserved sequence in the promoters of cold-responsive PR genes, such as PR1, PR2, and PR5. While transgenic plants overexpressing an active NTL6 form exhibited enhanced disease resistance, RNAi plants with reduced NTL6 activity were more susceptible to pathogen infection at low temperatures. Accordingly, cold induction of PR1 disappeared in the RNAi plants. Consistent with the close relationship between cold and pathogenesis, cold-acclimated plants showed enhanced resistance to pathogen infection. In this signaling cascade, controlled activation of the membrane-tethered, dormant NTL6 transcription factor serves as a molecular link that incorporates cold signals into pathogen resistance responses. However, the NTL6-mediated cold induction of the PR genes is independent of salicylic acid (SA). The PR genes were still induced by SA in the NTL6 RNAi plants. Cold regulation of the PR genes through the membrane-mediated transcriptional control is thought to be an adaptive process that ensures quick plant responses to incoming pathogens that frequently occur during cold seasons.

252 citations

Journal ArticleDOI
TL;DR: The results demonstrate that Arabidopsis can be used as model to unravel the genetics of Ve1-mediated resistance and show that signaling components utilized by Ve1 inArabidopsis to establish Verticillium resistance overlap with those required in tomato and include SERK3/BAK1, EDS1, and NDR1, which strongly suggests that critical components for resistance signaling are conserved.
Abstract: Vascular wilts caused by soil-borne fungal species of the Verticillium genus are devastating plant diseases. The most common species, Verticillium dahliae and Verticillium albo-atrum, have broad host ranges and are notoriously difficult to control. Therefore, genetic resistance is the preferred method for disease control. Only from tomato (Solanum lycopersicum) has a Verticillium resistance locus been cloned, comprising the Ve1 gene that encodes a receptor-like protein-type cell surface receptor. Due to lack of a suitable model for receptor-like protein (RLP)-mediated resistance signaling in Arabidopsis (Arabidopsis thaliana), so far relatively little is known about RLP signaling in pathogen resistance. Here, we show that Ve1 remains fully functional after interfamily transfer to Arabidopsis and that Ve1-transgenic Arabidopsis is resistant to race 1 but not to race 2 strains of V. dahliae and V. albo-atrum, nor to the Brassicaceae-specific pathogen Verticillium longisporum. Furthermore, we show that signaling components utilized by Ve1 in Arabidopsis to establish Verticillium resistance overlap with those required in tomato and include SERK3/BAK1, EDS1, and NDR1, which strongly suggests that critical components for resistance signaling are conserved. We subsequently investigated the requirement of SERK family members for Ve1 resistance in Arabidopsis, revealing that SERK1 is required in addition to SERK3/BAK1. Using virus-induced gene silencing, the requirement of SERK1 for Ve1-mediated resistance was confirmed in tomato. Moreover, we show the requirement of SERK1 for resistance against the foliar fungal pathogen Cladosporium fulvum mediated by the RLP Cf-4. Our results demonstrate that Arabidopsis can be used as model to unravel the genetics of Ve1-mediated resistance.

252 citations

Journal ArticleDOI
TL;DR: The objectives were to describe major bean disease problems in the Americas and review progress achieved in breeding for resistance and describe strategies to integrate genetic improvement for resistance to multiple diseases with cultivar development.
Abstract: Diseases cause severe losses (20–100%) to yield and quality of common bean (Phaseolus vulgaris L.) worldwide. Our objectives were to describe major bean disease problems in the Americas and review progress achieved in breeding for resistance. We also describe strategies to integrate genetic improvement for resistance to multiple diseases with cultivar development. Common bacterial blight, halo blight, and bacterial brown spot are the major bacterial diseases. Angular leaf spot, anthracnose, root rots, rust, and white mold are severe fungal diseases. Bean common mosaic virus (BCMV), Bean golden mosaic virus (BGMV), Bean golden yellow mosaic virus (BGYMV), and Beet curly top virus (BCTV) are important viral diseases. Breeding for resistance to one or two diseases at a time is emphasized. Backcross, pedigree, and bulk-pedigree methods of breeding are used. The use of molecular markers has gradually increased. Substantial progress has been made in breeding and genetics of resistance to most of these diseases; however, improvement in resistance to bacterial brown spot, halo blight, root rots, and web blight has been slow and localized. Furthermore, cultivars with high levels of resistance to one or more quantitatively inherited diseases (e.g., common bacterial blight and white mold) are rare. Breeding strategies for simultaneous and integrated genetic improvement of multiple qualitatively and quantitatively inherited resistances and cultivar development are briefly described.

251 citations

Journal ArticleDOI
TL;DR: The data reported so far support the idea that model II rather than model I is the realistic one, which revealed that populations with a polygenic resistance based on the gene-for-gene action have an increased level of resistance compared with the addition model, while its stability as far as mutability of the pathogen is concerned is higher compared to those with an additive gene action.
Abstract: Horizontal, uniform, race-non-specific or stable resistance can be discerned according to Van der Plank, from vertical, differential, race-specific or unstable resistance by a test in which a number of host genotypes (cultivars or clones) are tested against a number of pathogen genetypes traces of isolatest If the total non-environmental variance in levels of resistance is due to main effects only differences between cultivars and differences between isolates) the resistance and the pathogen many (in the broad sense) are horizontal in nature Vertical resistance and pathogenicity are characterized by the interaction between host and pathogen showing up as a variance compenent in this test due to interaction between cultivars and isolates A host and pathogen model was made in which resistance and pathogenicity are governed by live polygenic loci Within the host the resistance genes show additivity Two models were investigated in model I resistance and pathogenicity genes operate in an additive way as envisaged by Van der Plank in his horizontal resistance Model II is characterized by a gene-for-gene action between the polygenes of the host and those of the pathogen The cultivar isolate test in model I showed only main effect variance Surprisingly, the variance in model II was also largely due to main effects The contribution of the interaction to the variance uppeared so small, that it would be difficult to discern it from a normal error variance So-called horizontal resistance can therefore be explained by a polygenic resistance, where the individual genes are vertical and operating on a gene-for-gene basis with virulence genes in the pathogen The data reported so far support the idea that model II rather than model I is the realistic one The two models also revealed that populations with a polygenic resistance based on the gene-for-gene action have an increased level of resistance compared with the addition model, while its stability as far as mutability of the pathogen is concerned, is higher compared to those with an additive gene action Mathematical studies of Mode too support the gene-for-gene concept The operation of all resistance and virulence genes in a natural population is therefore seen as one integrated system All genes for true resistance in the host population, whether they are major or minor genes are considered to interact in a gene-for-gene way with virulence genes either major or minor, in the pathogen population The models revealed other important aspects Populations with a polygenic resistance based on a gene-for-gene action have an increased level of resistance compared to populations following the addition model The stability, as far as mutability of the pathogen is concerned, is higher in the interaction model than in the addition model The effect of a resistance gene on the level of resistance of the population consists of its effect on a single plant times its gene frequency in the population Due to the adaptive forces in both the host and the pathogen population and the gene-for-gene nature of the gene action an equilibrium develops that allows all resistance genes to remain effective although their corresponding virulence genes are present The frequencies of the resistance and virulence genes are such that the effective frequencies of resistance genes tend to be negatively related to the magnitude of the gene effect This explains why major genes often occur at low frequencies, while minor genes appear to be frequent It is in this way that the host and the pathogen, both as extremely variable and vigorous populations, can co-exist Horizontal and vertical resistance as meant by Van der Plank therefore do not represent different kinds of resistances, they represent merely polygenic and oligogenic resistances resp In both situations the individual host genes interact specifically with virulence genes in the pathogen Van der Plank's test for horizontal resistance appears to be a simple and sound way to test for polygenic inheritance of resistance The practical considerations have been discussed The agro-ecosystems should be made as diverse as possible Multilines, polygenic resistance, tolerance, gene deployment and other measures should be employed, if possible in combination

251 citations


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