Calcium‐dependent protein kinase 5 links calcium signaling with N ‐hydroxy‐ l ‐pipecolic acid‐ and SARD 1 ‐dependent immune memory in systemic acquired resistance

Summary Systemic acquired resistance ( SAR ) prepares infected plants for faster and stronger defense activation upon subsequent attacks. SAR requires an information relay from primary infection to distal tissue and the initiation and maintenance of a self‐maintaining phytohormone salicylic acid ( SA )‐defense loop. In spatial and temporal resolution, we show that calcium‐dependent protein kinase CPK 5 contributes to immunity and SAR . In local basal resistance, CPK 5 functions upstream of SA synthesis, perception, and signaling. In systemic tissue, CPK 5 signaling leads to accumulation of SAR ‐inducing metabolite N ‐hydroxy‐ L ‐pipecolic acid ( NHP ) and SAR marker genes, including Systemic Acquired Resistance Deficient 1 ( SARD 1) Plants of increased CPK 5, but not CPK 6, signaling display an ‘enhanced SAR ’ phenotype towards a secondary bacterial infection. In the sard1‐1 background, CPK 5‐mediated basal resistance is still mounted, but NHP concentration is reduced and enhanced SAR is lost. The biochemical analysis estimated CPK 5 half maximal kinase activity for calcium, K50 [Ca 2+ ], to be c . 100 nM, close to the cytoplasmic resting level. This low threshold uniquely qualifies CPK 5 to decode subtle changes in calcium, a prerequisite to signal relay and onset and maintenance of priming at later time points in distal tissue. Our data explain why CPK 5 functions as a hub in basal and systemic plant immunity.