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.
Highlights
Plants are protected from pathogen attack through activation of innate immune system, which is a consequence of co-evolution between plants and their pathogens (Jones and Dangl, 2006)
We previously found in Arabidopsis that B. cereus AR156 could prime the whole plant for an induced resistance to Pst DC3000 infection
In agreement with the reduced disease symptom observed on leaf surface, significantly reduced fungal hyphae were detected inside leaf tissue from AR156pretreated plants than that with control pre-treatment, indicating AR156 effectively protected Arabidopsis from B. cinerea infection (Figure 1C)
Summary
Plants are protected from pathogen attack through activation of innate immune system, which is a consequence of co-evolution between plants and their pathogens (Jones and Dangl, 2006). Induced Systemic Resistance by AR156 molecules known as pathogen-associated molecular patterns (PAMPs), which include flagellin, lipopolysaccharides, glycoproteins, or chitin (Jones and Dangl, 2006). During the course of evolution, some successful pathogens emerged that can successfully infect plants by suppressing PTI. This suppression is achieved by secreting virulent proteins generically termed effectors, which causes effector-triggered susceptibility (ETS) (Speth et al, 2007). ETI usually is accompanied with a hypersensitive response (HR) at the infection site, which is thought to restrict biotrophic pathogen growth (Chisholm et al, 2006; Jones and Dangl, 2006)
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