Slymir482e-3p Mediates Tomato Wilt Disease By Modulating Ethylene Response Pathway

Fusarium oxysporum f. sp. Lycopersici, a necrotrophic pathogen, is a causal agent of tomato wilt disease. Plants have two major sophisticated innate immune systems, Pathogen-Associated Molecular Pattern (PAMP)-triggered immunity (PTI) and Effector-Triggered Immunity (ETI), to perceive and resist pathogen offenses (Jones and Dangl 2006). MicroRNAs (miRNAs) contribute to PTI and ETI by fine-tuning plant hormones and/or silencing the genes involved in pathogen virulence by regulating the expression of target genes, thereby acting as crucial regulators of the plant immune system (Fei et al. 2016). Many plants produce microRNAs belonging to the miRNA482/2118 superfamily. These miRNAs target R-genes of the class NBS-LRR (nucleotide binding site-leucine rich repeat) through recognizing the P-loop motif in the NBS-LRR mRNA. Our previous studies showed that SlymiR482e-3p, a members of the miR482/2118 superfamily in tomato, negatively regulated the resistance to Fusarium oxysporum f. sp. lycopersici (race 2) (Fol) by targeting several NBS-LRR genes (Ouyang et al. 2014). However, the exact mechanism underlying the basic function of SlymiR482e-3p during the response to Fol attack needs further exploration. In this study, two near-isogenic tomato cultivars, Moneymaker (susceptible, i-2/i-2) and Motelle (resistant, I-2/I-2) to Fol infection, were recruited (Ouyang et al. 2014).