College of Horticulture, Nanjing Agricultural University, Nanjing, Jiangsu 210095, PR China.
College of Horticulture, Nanjing Agricultural University, Nanjing, Jiangsu 210095, PR China; Xuzhou Institute of Agricultural Sciences in Jiangsu Xuhuai District, Xuzhou, Jiangsu 221131, PR China.
Plant Sci. 2024 Apr;341:112008. doi: 10.1016/j.plantsci.2024.112008. Epub 2024 Feb 1.
miRNAs govern gene expression and regulate plant defense. Alternaria alternata is a destructive fungal pathogen that damages apple. The wild apple germplasm Malus hupehensis is highly resistant to leaf spot disease caused by this fungus. Herein, we elucidated the regulatory and functional role of miR393a in apple resistance against A. alternata by targeting Transport Inhibitor Response 1. Mature miR393 accumulation in infected M. hupehensis increased owing to the transcriptional activation of MIR393a, determined to be a positive regulator of A. alternata resistance to either 'Orin' calli or 'Gala' leaves. 5' RLM-RACE and co-transformation assays showed that the target of miR393a was MhTIR1, a gene encoding a putative F-box auxin receptor that compromised apple immunity. RNA-seq analysis of transgenic calli revealed that MhTIR1 upregulated auxin signaling gene transcript levels and influenced phytohormone pathways and plant-pathogen interactions. miR393a compromised the sensitivity of several auxin-signaling genes to A. alternata infection, whereas MhTIR1 had the opposite effect. Using exogenous indole-3-acetic acid or the auxin synthesis inhibitor L-AOPP, we clarified that auxin enhances apple susceptibility to this pathogen. miR393a promotes SA biosynthesis and impedes pathogen-triggered ROS bursts by repressing TIR1-mediated auxin signaling. We uncovered the mechanism underlying the miR393a-TIR1 module, which interferes with apple defense against A. alternata by modulating the auxin signaling pathway.
miRNAs 调控基因表达并调节植物防御。链格孢是一种破坏性的真菌病原体，可损害苹果。野生苹果种质资源绵刺极易感染由这种真菌引起的叶斑病。在此，我们通过靶向运输抑制剂响应 1 阐明了 miR393a 在苹果抵抗链格孢中的调控和功能作用。由于 MIR393a 的转录激活，感染的绵刺中成熟 miR393 的积累增加，被确定为对‘Orin’愈伤组织或‘Gala’叶片中 A. alternata 抗性的正调节剂。5' RLM-RACE 和共转化测定表明，miR393a 的靶标是 MhTIR1，该基因编码一个假定的 F-box 生长素受体，削弱了苹果的免疫力。转基因愈伤组织的 RNA-seq 分析表明，MhTIR1 上调了生长素信号基因的转录水平，并影响了植物激素途径和植物-病原体相互作用。miR393a 降低了几种生长素信号基因对 A. alternata 感染的敏感性，而 MhTIR1 则有相反的作用。使用外源吲哚-3-乙酸或生长素合成抑制剂 L-AOPP，我们阐明了生长素增强了苹果对这种病原体的易感性。miR393a 通过抑制 TIR1 介导的生长素信号来促进 SA 生物合成并阻止病原体引发的 ROS 爆发。我们揭示了 miR393a-TIR1 模块的作用机制，该模块通过调节生长素信号通路干扰了苹果对 A. alternata 的防御。
