Genotypic Variation in Resistance Gene-Mediated Calcium Signaling and Hormonal Signaling Involved in Effector-Triggered Immunity or Disease Susceptibility in the Pv. - Pathosystem

To characterize cultivar variation in resistance gene (R-gene)-mediated calcium signaling and hormonal regulation in effector-triggered immunity (ETI) and disease susceptibility, pv. () was inoculated in two cultivars (cvs. Capitol and Mosa). At 14 days post inoculation (DPI) with , there was a necrotic lesion in cv. Mosa along with the significant accumulation of HO and malondialdehyde (MDA), whereas no visual symptom was observed in cv. Capitol. The cultivar variations in the R-gene expressions were found in response to . is a coiled-coil-nucleotide binding site-leucine-rich repeat (CC-NB-LRR)-type R-gene that is significantly induced in cv. Capitol, whereas toll/interleukin-1 receptor-nucleotide binding site-leucine-rich repeat (TIR-NB-LRR)-type R-gene, , is significantly upregulated in cv. Mosa -inoculated plants. The defense-related gene's non-race-specific disease resistance 1 () and mitogen-activated protein kinase 6 () were enhanced, whereas calcium-dependent protein kinase () and calcium-sensing protein 60g ( were depressed in cv. Capitol inoculated plants, and opposite results were found in cv. Mosa. The calcium-sensing receptor (), calmodulin (), expression was induced in both the cultivars. However, the induction rate was much higher in cv. Mosa than in cv. Capitol in response to . The phytohormone salicylic acid (SA) and jasmonic acid (JA) levels were significantly higher in cv. Capitol along with the enhanced SA receptors ( and ) and JA synthesis and signaling-related gene expression (), whereas the JA level was significantly lower in cv. Mosa inoculated plants. The SA synthesis and signaling-related genes () and SA were present at higher levels in cv. Mosa; additionally, the SA level present was much higher in the susceptible cultivar (cv. Mosa) than in the resistant cultivar (cv. Capitol) in response to . These results indicate that mediated the coordinated action of SA and JA synthesis and signaling to confirm ETI, whereas enhanced the synthesis of SA through and to antagonize JA synthesis and signaling to cause disease susceptibility in the - pathosystem.