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Calcium-dependent protein kinase 5 links calcium-signaling with N-Hydroxy-L-pipecolic acid- and SARD1-dependent immune memory in systemic acquired resistance.

Tiziana Guerra,Silke M. Schilling,Katharina Hake,K. Gorzolka,F. Sylvester,B. Conrads,B. Westermann,T. Romeis

Published 2019 in New Phytologist

ABSTRACT

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 CPK5 contributes to immunity and SAR. In local basal resistance CPK5 functions upstream of SA-synthesis, -perception, and -signaling. In systemic tissue, CPK5 signaling leads to accumulation of SAR inducing metabolite N-Hydroxy-L-pipecolic acid (NHP) and SAR marker genes including Systemic Acquired Resistance Deficient 1 (SARD1) Plants of increased CPK5-, but not CPK6- signaling, display an 'enhanced SAR' phenotype toward a secondary bacterial infection. In sard1-1 background, CPK5-mediated basal resistance is still mounted, but NHP level is reduced and 'enhanced SAR' is lost. The biochemical analysis determines CPK5 half maximal kinase activity for calcium K50 [Ca2+ ] to ~100 nM close to the cytoplasmic resting level. This low threshold uniquely qualifies CPK5 to decode subtle changes in calcium prerequisite to signal relay and onset and maintenance of priming at later time points in distal tissue. Our data explain why CPK5 functions as a hub in basal and systemic plant immunity. This article is protected by copyright. All rights reserved.

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