Topic
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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TL;DR: The Mi locus of tomato confers resistance to root knot nematodes, and three open reading frames were identified with similarity to cloned plant disease resistance genes, including Prf, a tomato gene required for resistance to Pseudomonas syringae.
Abstract: The Mi locus of tomato confers resistance to root knot nematodes. Tomato DNA spanning the locus was isolated as bacterial artificial chromosome clones, and 52 kb of contiguous DNA was sequenced. Three open reading frames were identified with similarity to cloned plant disease resistance genes. Two of them, Mi-1.1 and Mi-1.2, appear to be intact genes; the third is a pseudogene. A 4-kb mRNA hybridizing with these genes is present in tomato roots. Complementation studies using cloned copies of Mi-1.1 and Mi-1.2 indicated that Mi-1.2, but not Mi-1.1, is sufficient to confer resistance to a susceptible tomato line with the progeny of transformants segregating for resistance. The cloned gene most similar to Mi-1.2 is Prf, a tomato gene required for resistance to Pseudomonas syringae. Prf and Mi-1.2 share several structural motifs, including a nucleotide binding site and a leucine-rich repeat region, that are characteristic of a family of plant proteins, including several that are required for resistance against viruses, bacteria, fungi, and now, nematodes.
753 citations
TL;DR: The ability of nim1 plants to support growth of normally incompatible races of a fungal pathogen indicates a role for this pathway in expression of genetically determined resistance, consistent with earlier findings for transgenic plants engineered to break down SA.
Abstract: Plants possess multiple resistance mechanisms that guard against pathogen attack. Among these are inducible systems such as systemic acquired resistance (SAR). SAR is activated by pathogen exposure and leads to an increase in salicylic acid (SA), high-level expression of SAR-related genes, and resistance to a spectrum of pathogens. To identify components of the signal transduction pathways regulating SAR, a mutant screen was developed that uses 2,6-dichloroisonicotinic acid as an activator of SAR gene expression and pathogen resistance, followed by assays for resistance to the fungal pathogen Peronospora parasitica. Mutants from this screen were subsequently examined to assess their defense responses. We describe here a recessive mutation that causes a phenotype of insensitivity to chemical and biological inducers of SAR genes and resistance. These data indicate the existence of a common signaling pathway that couples these diverse stimuli to induction of SAR genes and resistance. Because of its non-inducible immunity phenotype, we call this mutant nim1. Although nim1 plants fail to respond to SA, they retain the ability to accumulate wild-type levels of SA, a probable endogenous signal for SAR. Further, the ability of nim1 plants to support growth of normally incompatible races of a fungal pathogen indicates a role for this pathway in expression of genetically determined resistance, consistent with earlier findings for transgenic plants engineered to break down SA. These results suggest that the wild-type NIM1 gene product functions in a pathway regulating acquired resistance, at a position downstream of SA accumulation and upstream of SAR gene induction and expression of resistance.
745 citations
TL;DR: Out of 25 genotypes tested, five were identified with no significant difference in head blight scores, but differing significantly in yield after artificial inoculation, i.e. tolerance differences were detected at different resistance levels.
Abstract: Resistance of wheat to Fusarium head blight caused by Fusarium graminearum and F. culmorum was identified in natural epidemics in 1985 and 1987 as well after artificial inoculations (1983–1988 and 1984–1987). Out of 25 genotypes tested, five were identified with no significant difference in head blight scores, but differing significantly in yield after artificial inoculation, i.e. tolerance differences were detected at different resistance levels. Some genotypes that were similar in yield or head blight scores differed in seed infection severity. Genotypes with awns were more susceptible to head blight when tested under natural epidemic condition in the field; but this trait did not influence head blight severity in artificial inoculations. Dwarf genotypes were more severely infected by head blight than tall genotypes under natural conditions, but genotypes of different plant height classes were similarly susceptible after artificial inoculations. In the early generations of a breeding programme resistance measured by visual evaluation of artificial inoculation is the most important way to screen. If selection of dwarf and awned genotypes cannot be avoided, the higher susceptibility caused by awns and dwarfness under natural epidemic conditions can be decreased by a higher level of physiological resistance, as variability in physiological resistance is available. In later generations, traits like percentage of seed infection or tolerance can be identified by additionally measuring yield reduction. Stability of disease reaction appears to be connected with resistance level, the most resistant genotypes are the most stable, and the most susceptible ones tend to have more unstable reactions in different epidemic conditions.
720 citations
TL;DR: Six Arabidopsis mutants are described, defining at least four loci, that spontaneously form necrotic lesions on leaves, a novel mutant class Isd (for lesions simulating disease resistance response) that varies in cell type preferences for lesion onset and spread.
716 citations
TL;DR: X. oryzae pathovars with rice present as models for understanding fundamental aspects of bacterial pathogenesis of plants and plant disease resistance, as well as other aspects of plant and microbial biology, with implications also for animal innate immunity.
Abstract: SUMMARY Xanthomonas oryzae pv. oryzae and Xanthomonas oryzae pv. oryzicola cause bacterial blight and bacterial leaf streak of rice (Oryza sativa), which constrain production of this staple crop in much of Asia and parts of Africa. Tremendous progress has been made in characterizing the diseases and breeding for resistance. X. oryzae pv. oryzae causes bacterial blight by invading the vascular tissue, while X. oryzae pv. oryzicola causes bacterial leaf streak by colonizing the parenchyma. In rice there are 29 major genes for resistance to bacterial blight, but so far only a few quantitative resistance loci for bacterial leaf streak. Over 30 races of X. oryzae pv. oryzae have been reported. Both pathogens exhibit genetic variation among isolates. Mechanisms of pathogenesis and resistance have begun to be elucidated. Members of the AvrBs3/PthA family of transcription activator-like effectors play a major role in the virulence of X. oryzae pv. oryzae and possibly X. oryzae pv. oryzicola. Cloning of six rice resistance genes for bacterial blight and one from maize effective against bacterial leaf streak has uncovered a diversity of structure and function, some shared by genes involved in defence in animals. This article reviews research that spans a century. It also presents a perspective on challenges for sustainable control, and opportunities that interactions of X. oryzae pathovars with rice present as models for understanding fundamental aspects of bacterial pathogenesis of plants and plant disease resistance, as well as other aspects of plant and microbial biology, with implications also for animal innate immunity.
716 citations