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Effector-triggered innate immunity contributes Arabidopsis resistance to Xanthomonas campestris.

ABSTRACT: Xanthomonas campestris pv. campestris, the causal agent of black rot disease, depends on its type III secretion system (TTSS) to infect cruciferous plants, including Brassica oleracea, B. napus and Arabidopsis. Previous studies on the Arabidopsis-Pseudomonas syringae model pathosystem have indicated that a major function of TTSS from virulent bacteria is to suppress host defences triggered by pathogen-associated molecular patterns. Similar analyses have not been made for the Arabidopsis-X. campestris pv. campestris pathosystem. In this study, we report that X. campestris pv. campestris strain 8004, which is modestly pathogenic on Arabidopsis, induces strong defence responses in Arabidopsis in a TTSS-dependent manner. Furthermore, the induction of defence responses and disease resistance to X. campestris pv. campestris strain 8004 requires NDR1 (NON-RACE-SPECIFIC DISEASE RESISTANCE1), RAR1 (required for Mla12 resistance) and SGT1b (suppressor of G2 allele of skp1), suggesting that effector-triggered immunity plays a large role in resistance to this strain. Consistent with this notion, AvrXccC, an X. campestris pv. campestris TTSS effector protein, induces PR1 expression and confers resistance in Arabidopsis in a RAR1- and SGT1b-dependent manner. In rar1 and sgt1b mutants, AvrXccC acts as a virulence factor, presumably because of impaired resistance gene function.

SUBMITTER: Rong W

PROVIDER: S-EPMC6640269 | biostudies-literature | 2010 Nov

REPOSITORIES: biostudies-literature

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Effector-triggered innate immunity contributes Arabidopsis resistance to Xanthomonas campestris.

Rong Wei W Feng Feng F Zhou Jianmin J He Chaozu C

Molecular plant pathology 20101101 6

Xanthomonas campestris pv. campestris, the causal agent of black rot disease, depends on its type III secretion system (TTSS) to infect cruciferous plants, including Brassica oleracea, B. napus and Arabidopsis. Previous studies on the Arabidopsis-Pseudomonas syringae model pathosystem have indicated that a major function of TTSS from virulent bacteria is to suppress host defences triggered by pathogen-associated molecular patterns. Similar analyses have not been made for the Arabidopsis-X. campe ...[more]

PMID: 21029323

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Project description: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.

Project description:To characterize cultivar variations in hormonal regulation of the transition between pattern-triggered immunity (PTI) and effector-triggered immunity or susceptibility (ETI or ETS), the responses of resistance (R-) genes, hydrogen peroxide, and proline metabolism in two Brassica napus cultivars to contrasting disease susceptibility (resistant cv. Capitol vs. susceptible cv. Mosa) were interpreted as being linked to those of endogenous hormonal levels and signaling genes based on a time course of disease symptom development. Disease symptoms caused by the Xanthomonas campestris pv. campestris (Xcc) infections were much more developed in cv. Mosa than in cv. Capitol, as shown by an earlier appearance (at 3 days postinoculation [3 DPI]) and larger V-shaped necrosis lesions (at 9-15 DPI) in cv. Mosa. The cultivar variations in the R-genes, hormone status, and proline metabolism were found in two different phases (early [0-3 DPI] and later [9-15 DPI]). In the early phase, Xcc significantly upregulated PTI-related cytoplasmic kinase (Botrytis-induced kinase-1 [BIK1]) expression (+6.3-fold) with salicylic acid (SA) accumulation in cv. Capitol, while relatively less (+2.6-fold) with highly increased jasmonic acid (JA) level in cv. Mosa. The Xcc-responsive proline accumulation in both cultivars was similar to upregulated expression of proline synthesis-related genes (P5CS2 and P5CR). During the later phase in cv. Capitol, Xcc-responsive upregulation of ZAR1 (a coiled-coil-nucleotide binding site-leucine-rich repeat [CC-NB-LRR-type R-gene]) was concomitant with a gradual increase in JA levels without additional proline accumulation. However, in cv. Mosa, upregulation of TAO1 (a toll/interleukin-1 receptor-nucleotide binding site-leucine-rich repeat [TIR-NB-LRR-type R-gene]) was consistent with an increase in SA and abscisic acid (ABA) levels and resulted in an antagonistic depression of JA, which led to a proline accumulation. These results indicate that Xcc-induced BIK1- and ZAR1-mediated JA signaling interactions provide resistance and confirm ETI, whereas BIK1- and TAO1-enhanced SA- and/or ABA-mediated proline accumulation is associated with disease susceptibility (ETS).

Dataset Information

Effector-triggered innate immunity contributes Arabidopsis resistance to Xanthomonas campestris.

Publications

Effector-triggered innate immunity contributes Arabidopsis resistance to Xanthomonas campestris.

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