N-hydroxypipecolic acid-induced transcription requires the salicylic acid signaling pathway at basal SA levels

• Published in: Plant physiology (Bethesda) Vol. 187; no. 4; pp. 2803 - 2819
• Main Authors: Nair, Aswin, Goyal, Isha, Voß, Edgar, Mrozek, Pascal, Prajapati, Sabin, Thurow, Corinna, Tietze, Lutz, Tittmann, Kai, Gatz, Christiane
• Format: Journal Article
• Language: English
• Published: United States Oxford University Press 04.12.2021
• Subjects: Arabidopsis - genetics; Arabidopsis - physiology; Gene Expression Regulation, Plant; Pipecolic Acids - metabolism; Regular Issue; Salicylic Acid - metabolism; Signal Transduction; Transcription, Genetic
• ISSN: 0032-0889; 1532-2548
• DOI: 10.1093/plphys/kiab433

Systemic acquired resistance (SAR) is a plant immune response established in uninfected leaves after colonization of local leaves with biotrophic or hemibiotrophic pathogens. The amino acid-derived metabolite N-hydroxypipecolic acid (NHP) travels from infected to systemic leaves, where it activates salicylic acid (SA) biosynthesis through the isochorismate pathway. The resulting increased SA levels are essential for induction of a large set of SAR marker genes and full SAR establishment. In this study, we show that pharmacological treatment of Arabidopsis thaliana with NHP induces a subset of SAR-related genes even in the SA induction-deficient2 (sid2/isochorismate synthase1) mutant, which is devoid of NHP-induced SA. NHP-mediated induction is abolished in sid2-1 NahG plants, in which basal SA levels are degraded. The SA receptor NON-EXPRESSOR OF PATHOGENESIS-RELATED GENES1 (NPR1) and its interacting TGACG SEQUENCE-SPECIFIC BINDING PROTEIN (TGA) transcription factors are required for the NHP-mediated induction of SAR genes at resting SA levels. Isothermal titration analysis determined a KD of 7.9 ± 0.5 µM for the SA/NPR1 complex, suggesting that basal levels of SA would not bind to NPR1 unless yet unknown potentially NHP-induced processes increase the affinity. Moreover, the nucleocytoplasmic protein PHYTOALEXIN DEFICIENT4 is required for a slight NHP-mediated increase in NPR1 protein levels and NHP-induced expression of SAR-related genes. Our experiments have unraveled that NHP requires basal SA and components of the SA signaling pathway to induce SAR genes. Still, the mechanism of NHP perception remains enigmatic.