Induced Systemic Resistance against Botrytis cinerea by Bacillus cereus AR156 through a JA/ET- and NPR1-Dependent Signaling Pathway and Activates PAMP-Triggered Immunity in Arabidopsis

Abstract

Induced resistance response is a potent and cost effective plant defense against pathogen attack. The effectiveness and underlying mechanisms of the suppressive ability by Bacillus cereus AR156 to Pseudomonas syringae pv. tomato DC3000 (Pst DC3000) in Arabidopsis has been investigated previously; however, the strength of induced systemic resistance (ISR) activity against Botrytis cinerea remains unknown. Here, we show that root-drench application of AR156 significantly reduces disease incidence through activation of ISR. This protection is accompanied with multilayered ISR defense response activated via enhanced accumulation of PR1 protein expression in a timely manner, hydrogen peroxide accumulation and callose deposition, which is significantly more intense in plants with both AR156 pretreatment and B. cinerea inoculation than that in plants with pathogen inoculation only. Moreover, AR156 can trigger ISR in sid2-2 and NahG mutants, but not in jar1, ein2 and npr1 mutant plants. Our results indicate that AR156-induced ISR depends on JA/ET-signaling pathway and NPR1, but not SA. Also, AR156-treated plants are able to rapidly activate MAPK signaling and FRK1/WRKY53 gene expression, both of which are involved in pathogen associated molecular pattern (PAMP)-triggered immunity (PTI). The results indicate that AR156 can induce ISR by the JA/ET-signaling pathways in an NPR1-dependent manner and involves multiple PTI components.

Plastic Transcriptomes Stabilize Immunity to Pathogen Diversity: The Jasmonic Acid and Salicylic Acid Networks within the Arabidopsis/Botrytis Pathosystem

“…This supports the perspective that host resistance to B. cinerea is extremely polygenic (Corwin et al, 2016a). Interestingly, three of the top 10 highest positively correlated genes encode a chitinase, a chitininducible gene (AT5G25260), and a PAMP-inducible kinase FRK1 (Passarinho et al, 2001;Millet et al, 2010;Yeh et al, 2016;Nie et al, 2017). A fourth gene in the top 10 is UGT76B1, which controls crosstalk between the SA and JA pathways (von Saint Paul et al, 2011).…”

Differential roles of melatonin in plant‐host resistance and pathogen suppression in cucurbits

“…hordei (powdery mildew) (Cla006906, Cla018026, Cla002075, Cla015613). Two of the DEGs, Cla021170 and Cla001623, are orthologs of genes required for incompatible interaction against plant pathogens in Arabidopsis . We also identified 4 genes (Cla021170, Cla002982, Cla012528, and Cla001623 ) that were strongly associated with innate immune response, which can directly recognize components of potential pathogens (MAMP/PAMP/effectors), suggesting a possible priming role in defense pathway.…”

“…Two of the DEGs, Cla021170 and Cla001623, are orthologs of genes required for incompatible interaction against plant pathogens in Arabidopsis. 79,80 We also identified 4 genes (Cla021170, Cla002982, Cla012528, and Cla001623) that were strongly associated with innate immune response, which can directly recognize components of potential pathogens (MAMP/PAMP/effectors), suggesting a possible priming role in defense pathway. The upregulated genes (Cla021170, Cla018126, Cla018026, Cla002075, Cla001623), which are known to be activated in response to salicylic acid, support previous research, indicating that the defense pathway initiated by melatonin is dependent on F I G U R E 2 Broad-spectrum effect of Melatonin on growth of Phytophthora capsici.…”

The cell-wall-localised BETA-XYLOSIDASE 4 contributes to immunity of Arabidopsis against Botrytis cinerea

“…We next assayed if the reduced expression of PDF1.2 and PAD3 in bxl4 mutants correlates with a reduced accumulation of JA-Ile and camalexin upon infection with B. cinerea (Figure 8) (Ferrari et al, 2003, 2007; Scalschi et al, 2015; Nie et al, 2017). The bxl4 mutants showed a slight reduction in JA-Ile abundance especially at 72 h post inoculation compared to Col-0 (Figure 8D).…”