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.

SNARE-protein-mediated disease resistance at the plant cell wall

Abstract: Failure of pathogenic fungi to breach the plant cell wall constitutes a major component of immunity of non-host plant species--species outside the pathogen host range--and accounts for a proportion of aborted infection attempts on 'susceptible' host plants (basal resistance). Neither form of penetration resistance is understood at the molecular level. We developed a screen for penetration (pen) mutants of Arabidopsis, which are disabled in non-host penetration resistance against barley powdery mildew, Blumeria graminis f. sp. hordei, and we isolated the PEN1 gene. We also isolated barley ROR2 (ref. 2), which is required for basal penetration resistance against B. g. hordei. The genes encode functionally homologous syntaxins, demonstrating a mechanistic link between non-host resistance and basal penetration resistance in monocotyledons and dicotyledons. We show that resistance in barley requires a SNAP-25 (synaptosome-associated protein, molecular mass 25 kDa) homologue capable of forming a binary SNAP receptor (SNARE) complex with ROR2. Genetic control of vesicle behaviour at penetration sites, and plasma membrane location of PEN1/ROR2, is consistent with a proposed involvement of SNARE-complex-mediated exocytosis and/or homotypic vesicle fusion events in resistance. Functions associated with SNARE-dependent penetration resistance are dispensable for immunity mediated by race-specific resistance (R) genes, highlighting fundamental differences between these two resistance forms.

Molecular genetics of plant disease resistance

Abstract: Plant breeders have used disease resistance genes (R genes) to control plant disease since the turn of the century. Molecular cloning of R genes that enable plants to resist a diverse range of pathogens has revealed that the proteins encoded by these genes have several features in common. These findings suggest that plants may have evolved common signal transduction mechanisms for the expression of resistance to a wide range of unrelated pathogens. Characterization of the molecular signals involved in pathogen recognition and of the molecular events that specify the expression of resistance may lead to novel strategies for plant disease control.

Structure of the Arabidopsis RPM1 gene enabling dual specificity disease resistance

Abstract: Plants can recognize pathogens through the action of disease resistance (R) genes, which confer resistance to pathogens expressing unique corresponding avirulence (avr) genes. The molecular basis of this gene-for-gene specificity is unknown. The Arabidopsis thaliana RPM1 gene enables dual specificity to pathogens expressing either of two unrelated Pseudomonas syringae avr genes. Despite this function, RPM1 encodes a protein sharing molecular features with recently described single-specificity R genes. Surprisingly, RPM1 is lacking from naturally occurring, disease-susceptible Arabidopsis accessions.

Tobacco Rar1, EDS1 and NPR1/NIM1 like genes are required for N‐mediated resistance to tobacco mosaic virus

Abstract: The tobacco N gene confers resistance to tobacco mosaic virus (TMV) and encodes a Toll-interleukin-1 receptor/nucleotide binding site/leucine-rich repeat (TIR-NBS-LRR) class protein. We have developed and used a tobacco rattle virus (TRV) based virus induced gene silencing (VIGS) system to investigate the role of tobacco candidate genes in the N-mediated signalling pathway. To accomplish this we generated transgenic Nicotiana benthamiana containing the tobacco N gene. The transgenic lines exhibit hypersensitive response (HR) to TMV and restrict virus spread to the inoculated site. This demonstrates that the tobacco N gene can confer resistance to TMV in heterologous N. benthamiana. We have used this line to study the role of tobacco Rar1-, EDS1-, and NPR1/NIM1- like genes in N-mediated resistance to TMV using a TRV based VIGS approach. Our VIGS analysis suggests that these genes are required for N function. EDS1-like gene requirement for the N function suggests that EDS1 could be a common component of bacterial, fungal and viral resistance signalling mediated by the TIR-NBS-LRR class of resistance proteins. Requirement of Rar1- like gene for N-mediated resistance to TMV and some powdery mildew resistance genes in barley provide the first example of converging points in the disease resistance signalling pathways mediated by TIR-NBS-LRR and CC-NBS-LRR proteins. The TRV based VIGS approach as described here to study N-mediated resistance signalling will be useful for the analysis of not only disease resistance signalling pathways but also of other signalling pathways in genetically intractable plant systems.

Active Oxygen Species in Plant Defense against Pathogens.

Abstract: Plant disease resistance to pathogens such as fungi, bacteria, and viruses often depends on whether the plant is able to recognize the pathogen early in the infection process. The recognition event leads to a rapid tissue necrosis at the site of infection, which is called the HR. The HR deprives the pathogen of nutrients and/or releases toxic molecules, thereby confining pathogen growth to a small region of the plant. This response provides resistance to the great majority of potential pathogens (nonhost or species resistance). For a given plant species, a much more limited number of true pathogens exhibit the ability to evade the host recognition system and grow extensively within the plant without evoking host necrosis at a11 or only after considerable delay. In this case, the plant exhibits susceptibility and the extensive growth of the successful pathogen can cause varying degrees of damage. However, certain races within pathogenic bacteria1 or funga1 species are recognized by certain cultivars or genotypes of the host plant species and the HR is triggered. These observations indicate that there is an ongqing evolution of the host plant's ability to recognize pathogen races that were previously unrecognized while the pathogen evolves to avoid recognition by a previously resistant host. Recognition of pathogens triggers a large range of inducible defense mechanisms that are believed to contribute to overall resistance in the plant. The mechanisms induced at the site of infection and associated with the HR include synthesis of antimicrobial compounds called phytoalexins, synthesis of hydrolytic enzymes that attack fungi and bacteria, and alterations in the synthesis of cell-wall structural proteins (for