Warm temperature suppresses plant systemic acquired resistance by intercepting theN-hydroxypipecolic acid immune pathway

Abstract

AbstractClimate warming influences disease development by targeting critical components of the plant immune system, including pattern-triggered immunity (PTI), effector-triggered immunity (ETI) and production of the central defence hormone salicylic acid (SA) at the primary pathogen infection site. However, it is not clear if and/or how temperature impacts systemic immunity. Here we show that pathogen-triggered systemic acquired resistance (SAR) inArabidopsis thalianais suppressed at elevated temperature. This was accompanied by global downregulation of SAR-induced genes at elevated temperature. Abolished SAR under warmer conditions was associated with reduced biosynthesis of the SAR metaboliteN-hydroxypipecolic acid (NHP) inArabidopsisand other plant species, as demonstrated by downregulation of NHP biosynthetic genes (ALD1andFMO1) and NHP precursor pipecolic acid (Pip) levels. Although multiple SAR signals have been shown previously, exogenous Pip was sufficient to restore disease protection at elevated temperature, indicating that heat-mediated SAR suppression is due to Pip-NHP downregulation. Along withALD1andFMO1, systemic expression of the SA biosynthetic geneICS1was also suppressed at warm temperature. Finally, we define a transcriptional network controlling thermosensitive NHP pathway via the master transcription factors CBP60g and SARD1. Our findings demonstrate that warm temperatures impact not only local but also systemic immunity by impinging on the NHP pathway, providing a roadmap towards engineering climate-resilient plant immune systems.