To characterize cultivar variation in resistance gene (R-gene)-mediated calcium signaling and hormonal regulation in effector-triggered immunity (ETI) and
disease susceptibility, Xanthomonas campestris pv. campestris (
Xcc) was inoculated in two Brassica napus cultivars (cvs. Capitol and Mosa). At 14 days post inoculation (DPI) with
Xcc, there was a necrotic lesion in cv. Mosa along with the significant accumulation of H2O2 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
Xcc. ZAR1 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, TAO1, is significantly upregulated in cv. Mosa
Xcc-inoculated plants. The defense-related gene's non-race-specific
disease resistance 1 (NDR1) and
mitogen-activated protein kinase 6 (MAPK6) were enhanced, whereas
calcium-dependent protein kinase (CDPK5) and
calcium-sensing
protein 60g (CBP60g) were depressed in cv. Capitol
Xcc inoculated plants, and opposite results were found in cv. Mosa. The
calcium-sensing receptor (CAS),
calmodulin (CaM), expression was induced in both the cultivars. However, the CAS induction rate was much higher in cv. Mosa than in cv. Capitol in response to
Xcc. The
phytohormone salicylic acid (SA) and
jasmonic acid (JA) levels were significantly higher in cv. Capitol along with the enhanced SA receptors (NPR3 and NPR4) and JA synthesis and signaling-related gene expression (LOX2, PDF1.2), whereas the JA level was significantly lower in cv. Mosa
Xcc inoculated plants. The SA synthesis and signaling-related genes (ICS1, NPR1) 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
Xcc. These results indicate that ZAR1 mediated the coordinated action of SA and JA synthesis and signaling to confirm ETI, whereas TAO1 enhanced the synthesis of SA through CAS and CBP60g to antagonize JA synthesis and signaling to cause
disease susceptibility in the Brassica napus-
Xcc pathosystem.