miR158a negatively regulates plant resistance to Phytophthora parasitica by repressing AtTN7 that requires EDS1-PAD4-ADR1 complex in Arabidopsis thaliana

Plant J. 2024 Dec 5. doi: 10.1111/tpj.17194. Online ahead of print.

Abstract

Small RNAs are involved in diverse cellular processes, including plant immunity to pathogens. Here, we report that miR158a negatively regulates plant immunity to the oomycete pathogen Phytophthora parasitica in Arabidopsis thaliana. By performing real-time quantitative PCR, transient expression, and RNA ligase-mediated 5' rapid amplification of cDNA ends assays, we demonstrate that miR158a downregulates AtTN7 expression by cleaving its 3'-untranslated region. AtTN7 positively affects plant immunity and encodes a truncated intracellular nucleotide-binding site and leucine-rich repeat receptor containing the Toll/interleukin-1 receptor. AtTN7 can degrade oxidized forms of nicotinamide adenine dinucleotide (NAD+). Further genetic and molecular analyses reveal that the Enhanced Disease Susceptibility 1-Phytoalexin Deficient 4-Activated Disease Resistance 1 complex is required for AtTN7-mediated immunity. ADR1-dependent Ca2+ influx is crucial for activating salicylic acid signaling to condition AtTN7-triggered immunity. Our study uncovers the immune roles and regulatory mechanisms of miR158a and its target AtTN7. Both miR158a-downregulation and AtTN7-overexpression lead to enhanced plant resistance to P. parasitica without affecting plant growth phenotypes, suggesting their application potentials and the utilization of miRNAs in identifying novel immune genes for the development of plant germplasm resources with enhanced disease resistance.

Keywords: Arabidopsis thaliana; AtTN7; Ca2+ influx; EDS1‐PAD4‐ADR1 complex; NAD+ degrade; Phytophthora parasitica; SA signaling; miR158a; plant immunity.