16-Systemic acquired resistance (SAR) prepares infected plants for faster and stronger 17 defense activation upon subsequent attacks. SAR requires an information relay from primary 18 infection to distal tissue and the initiation and maintenance of a self-maintaining 19 phytohormone salicylic acid (SA)-defense loop. 20 -In spatial and temporal resolution we show that calcium-dependent protein kinase CPK5 21 contributes to immunity and SAR. In local basal resistance CPK5 functions upstream of SA-22 synthesis, -perception, and -signaling. In systemic tissue, enhanced CPK5 signaling leads to 23 an accumulation of SAR marker genes including transcription factor Systemic Acquired 24Resistance Deficient 1 (SARD1). 25 -Plants of enhanced CPK5-, but not CPK6-, signaling display a 'super-priming' phenotype of 26 enhanced resistance toward a secondary bacterial infection. In sard1 background, CPK5-27 mediated basal resistance is still mounted but systemic 'super-priming' is lost. 28 -The biochemical analysis determines CPK5 half maximal kinase activity for calcium K50 29[Ca 2+ ] to ~100 nM close to the cytoplasmic resting level. This low activation threshold 30 uniquely qualifies CPK5 to decode subtle changes in calcium prerequisite to immune signal 31 relay and to onset and maintenance of priming at later time points in distal tissue. Our data 32 explain why CPK5 functions as a hub in basal and systemic plant immunity. 33 34

The calcium-dependent protein kinase CPK1 regulates a pivotal developmental switch in senescence and leaf cell death through direct phosphorylation of transcription factor ORE1.

As a critical part of plant immunity, cells that are attacked by pathogens undergo rapid transcriptional reprogramming to minimize virulence. Many bacterial phytopathogens use type III effector (T3E) proteins to interfere with plant defense responses, including this transcriptional reprogramming. Here, we show that XopS, a T3E of Xanthomonas campestris pv. vesicatoria (Xcv), interacts with and inhibits proteasomal degradation of WRKY40, a transcriptional regulator of defense gene expression. Virus-induced gene silencing of WRKY40 in pepper (Capsicum annuum) enhanced plant tolerance to Xcv infection, indicating that WRKY40 represses immunity. Stabilization of WRKY40 by XopS reduces the expression of its targets, which include salicylic acid (SA)-responsive genes and the jasmonic acid (JA) signaling repressor JAZ8. Xcv bacteria lacking XopS display significantly reduced virulence when surface inoculated onto susceptible pepper leaves. XopS delivery by Xcv, as well as ectopic expression of XopS in Arabidopsis thaliana or Nicotiana benthamiana, prevented stomatal closure in response to bacteria and biotic elicitors. Silencing WRKY40 in pepper or N. benthamiana abolished XopS’s ability to prevent stomatal closure. This suggests that XopS interferes with both preinvasion and apoplastic defense by manipulating WRKY40 stability and downstream gene expression, eventually altering phytohormone crosstalk to promote pathogen proliferation.