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.

Induced Disease Resistance in Plants by Chemicals

Abstract: Plants can be induced locally and systemically to become more resistant to diseases through various biotic or abiotic stresses. The biological inducers include necrotizing pathogens, non- pathogens or root colonizing bacteria. Through at network of signal pathways they induce resistance spectra and marker proteins that are characteristic for the different plant species and activation systems. The best characterized signal pathway for systemically induced resistance is SAR (systemic acquired resistance) that is activated by localized infections with necrotizing pathogens. It is characterized by protection against a broad range of pathogens, by a set of induced proteins and by its dependence on salicylic acid (SA) Various chemicals have been discovered that seem to act at various points in these defense activating networks and mimic all or parts of the biological activation of resistance. Of these, only few have reached commercialization. The best- studied resistance activator is acibenzolar-5-methyl (BION). At low rates it activates resistance in many crops against a broad spectrum of diseases, including fungi, bacteria and viruses. In monocots, activated resistance by BION typically is very long lasting, while the lasting effect is less pronounced in dicots. BION is translocated systemically in plants and can take the place of SA in the natural SAR signal pathway, inducing the same spectrum of resistance and the same set of molecular markers. Probenazole (ORYZEMATE) is used mainly on rice against rice blast and bacterial leaf blight. Its mode of action is not well understood partly because biological systems of systemically induced resistance are not well defined in rice. Treated plants clearly respond faster and in a resistant manner to infections by the two pathogens. Other compounds like beta-aminobutyric acid as wdl as extracts from plants and microorganisms have also been described as resistance inducers. For most of these, neither the mode of action nor reliable pre-challenge markers are known and still other pathways for resistance activation are suspected. Resistance inducing chemicals that are able to induce broad disease resistance offer an additional option for the farmer to complement genetic disease resistance and the use of fungicides. If integrated properly in plant health management programs, they can prolong the useful life of both the resistance genes and the fungicides presently used.

Positional Cloning of a Gene for Nematode Resistance in Sugar Beet

Abstract: The Hs1pro-1 locus confers resistance to the beet cyst nematode (Heterodera schachtii Schmidt), a major pest in the cultivation of sugar beet (Beta vulgaris L.). The Hs1pro-1 gene was cloned with the use of genome-specific satellite markers and chromosomal break-point analysis. Expression of the corresponding complementary DNA in a susceptible sugar beet conferred resistance to infection with the beet cyst nematode. The native Hs1pro-1 gene, expressed in roots, encodes a 282-amino acid protein with imperfect leucine-rich repeats and a putative membrane-spanning segment, features similar to those of disease resistance genes previously cloned from higher plants.

Interfamily transfer of a plant pattern-recognition receptor confers broad-spectrum bacterial resistance

Abstract: Plant diseases cause massive losses in agriculture. Increasing the natural defenses of plants may reduce the impact of phytopathogens on agricultural productivity. Pattern-recognition receptors (PRRs) detect microbes by recognizing conserved pathogen-associated molecular patterns (PAMPs). Although the overall importance of PAMP-triggered immunity for plant defense is established, it has not been used to confer disease resistance in crops. We report that activity of a PRR is retained after its transfer between two plant families. Expression of EFR (ref. 4), a PRR from the cruciferous plant Arabidopsis thaliana, confers responsiveness to bacterial elongation factor Tu in the solanaceous plants Nicotiana benthamiana and tomato (Solanum lycopersicum), making them more resistant to a range of phytopathogenic bacteria from different genera. Our results in controlled laboratory conditions suggest that heterologous expression of PAMP recognition systems could be used to engineer broad-spectrum disease resistance to important bacterial pathogens, potentially enabling more durable and sustainable resistance in the field.

Gene-for-gene disease resistance without the hypersensitive response in Arabidopsis dnd1 mutant

Abstract: The cell death response known as the hypersensitive response (HR) is a central feature of gene-for-gene plant disease resistance. A mutant line of Arabidopsis thaliana was identified in which effective gene-for-gene resistance occurs despite the virtual absence of HR cell death. Plants mutated at the DND1 locus are defective in HR cell death but retain characteristic responses to avirulent Pseudomonas syringae such as induction of pathogenesis-related gene expression and strong restriction of pathogen growth. Mutant dnd1 plants also exhibit enhanced resistance against a broad spectrum of virulent fungal, bacterial, and viral pathogens. The resistance against virulent pathogens in dnd1 plants is quantitatively less strong and is differentiable from the gene-for-gene resistance mediated by resistance genes RPS2 and RPM1. Levels of salicylic acid compounds and mRNAs for pathogenesis-related genes are elevated constitutively in dnd1 plants. This constitutive induction of systemic acquired resistance may substitute for HR cell death in potentiating the stronger gene-for-gene defense response. Although cell death may contribute to defense signal transduction in wild-type plants, the dnd1 mutant demonstrates that strong restriction of pathogen growth can occur in the absence of extensive HR cell death in the gene-for-gene resistance response of Arabidopsis against P. syringae.

DNA markers for Fusarium head blight resistance QTLs in two wheat populations

Abstract: Genetic resistance to Fusarium head blight (FHB), caused by Fusarium graminearum, is necessary to reduce the wheat grain yield and quality losses caused by this disease. Development of resistant cultivars has been slowed by poorly adapted and incomplete resistance sources and confounding environmental effects that make screening of germplasm difficult. DNA markers for FHB resistance QTLs have been identified and may be used to speed the introgression of resistance genes into adapted germplasm. This study was conducted to identify and map additional DNA markers linked to genes controlling FHB resistance in two spring wheat recombinant inbred populations, both segregating for genes from the widely used resistance source ’Sumai 3’. The first population was from the cross of Sumai 3/Stoa in which we previously identified five resistance QTLs. The second population was from the cross of ND2603 (Sumai 3/Wheaton) (resistant)/ Butte 86 (moderately susceptible). Both populations were evaluated for reaction to inoculation with F. graminearum in two greenhouse experiments. A combination of 521 RFLP, AFLP, and SSR markers were mapped in the Sumai 3/Stoa population and all DNA markers associated with resistance were screened on the ND2603/Butte 86 population. Two new QTL on chromosomes 3AL and 6AS wer found in the ND2603/Butte 86 population, and AFLP and SSR markers were identified that explained a greater portion of the phenotypic variation compared to the previous RFLP markers. Both of the Sumai 3-derived QTL regions (on chromosomes 3BS, and 6BS) from the Sumai 3/Stoa population were associated with FHB resistance in the ND2603/Butte 86 population. Markers in the 3BS QTL region (Qfhs.ndsu-3BS) alone explain 41.6 and 24.8% of the resistance to FHB in the Sumai 3/Stoa and ND2603/Butte 86 populations, respectively. This region contains a major QTL for resistance to FHB and should be useful in marker-assisted selection.