Genotypic Variation in Resistance Gene-Mediated Calcium Signaling and Hormonal Signaling Involved in Effector-Triggered Immunity or Disease Susceptibility in the Xanthomonas campestris pv. Campestris-Brassica napus Pathosystem.

Md Al Mamun,Dong-Won Bae,Tae-Hwan Kim,Bok-Rye Lee,Van Hien La,Md Tabibul Islam

doi:10.3390/plants9030303

Abstract

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.

Highlights

Black rot disease of oilseed rape (Brassica napus) caused by Xanthomonas campestris pv. campestris (Xcc) is a major threat that reduces the quality and productivity of Brassicaceae crops
Coiled-coil-nucleotide binding site-leucine-rich repeat (CC-NB-LRR) and toll/interleukin-1 receptor-nucleotide binding site-leucine-rich repeat (TIR-NB-LRR) are two major types of resistance gene (R-gene) that regulate the activation of the plant immune response, especially phytohormone signaling to counteract pathogenic infection [5]
H2 O2 is the primary detectable oxide that is capable of inducing cytosolic Ca2+ and calcium-dependent protein kinases (CDPKs) during pathogenic attack [4,6,7]

Summary

Introduction

Black rot disease of oilseed rape (Brassica napus) caused by Xanthomonas campestris pv. campestris (Xcc) is a major threat that reduces the quality and productivity of Brassicaceae crops. Campestris (Xcc) is a major threat that reduces the quality and productivity of Brassicaceae crops. Coiled-coil-nucleotide binding site-leucine-rich repeat (CC-NB-LRR) and toll/interleukin-1 receptor-nucleotide binding site-leucine-rich repeat (TIR-NB-LRR) are two major types of R-genes that regulate the activation of the plant immune response, especially phytohormone signaling to counteract pathogenic infection [5]. Reactive oxygen species (ROS) and calcium signaling play important roles in pattern-triggered immunity (PTI) or ETI [4]. H2 O2 is the primary detectable oxide that is capable of inducing cytosolic Ca2+ and calcium-dependent protein kinases (CDPKs) during pathogenic attack [4,6,7]. Phytohormone salicyclic acid (SA), a critical messenger, is induced for immune response during plant–pathogen interaction modulated by different Ca2+ signaling [8,9,10]

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Conclusion