Abstract
Root-knot nematodes, Meloidogyne spp., are important pests of tomato (Solanum lycopersicum) and resistance to the three most prevalent species of this genus, including Meloidogyne incognita, is mediated by the Mi-1 gene. Mi-1 encodes a nucleotide binding (NB) leucine-rich repeat (LRR) resistance (R) protein. Ethylene (ET) is required for the resistance mediated by a subset of NB-LRR proteins and its role in Mi-1-mediated nematode resistance has not been characterized. Infection of tomato roots with M. incognita differentially induces ET biosynthetic genes in both compatible and incompatible interactions. Analyzing the expression of members of the ET biosynthetic gene families ACC synthase (ACS) and ACC oxidase (ACO), in both compatible and incompatible interactions, shows differences in amplitude and temporal expression of both ACS and ACO genes in these two interactions. Since ET can promote both resistance and susceptibility against microbial pathogens in tomato, we investigated the role of ET in Mi-1-mediated resistance to M. incognita using both genetic and pharmacological approaches. Impairing ET biosynthesis or perception using virus-induced gene silencing (VIGS), the ET-insensitive Never ripe (Nr) mutant, or 1-methylcyclopropene (MCP) treatment, did not attenuate Mi-1-mediated resistance to M. incognita. However, Nr plants compromised in ET perception showed enhanced susceptibility to M. incognita indicating a role for ETR3 in basal resistance to root-knot nematodes.
Highlights
Plants have evolved different modes of defense to detect and limit pathogen invasion
Specific recognition of the invader by the plant host relies on the perception of pathogen associated molecular patterns (PAMPs), signatures that are characteristic of an entire class of pathogens [1,2]
ET signaling in tomato roots is activated during the early stages of RKN infection In a previous study [10], microarray analysis identified a large set of genes regulated in tomato roots in both resistant cv
Summary
Plants have evolved different modes of defense to detect and limit pathogen invasion. Physical damage or mechanical stress caused during the infection process can trigger plant defenses. Specific recognition of the invader by the plant host relies on the perception of pathogen associated molecular patterns (PAMPs), signatures that are characteristic of an entire class of pathogens [1,2]. In plants, this recognition triggers a chain of signaling events that leads to basal defense known as PAMPtriggered immunity (PTI). To evade PTI, pathogens have evolved effectors that interfere with recognition processes and/or suppress plant defenses. Plants have developed specific recognition factors or resistance (R) genes that directly or indirectly detect these effectors and trigger gene-for-gene resistance [3], known as effector-triggered immunity (ETI; [2])
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