Abstract

Non-host resistance (NHR) is a broad-spectrum plant defense. Upon colonizing on the surface on the root or leaves of non-host species, pathogens initial encounter preform and induce defense response in plant, such as induced hypersensitive response, PAMPs triggered immunity (PTI), and effector triggered immunity (ETI). The ability of plants to develop an induced systemic response (ISR) in reaction to the colonization by non-pathogenic rhizobacterium depends on interactions between host plants and the colonizing rhizobacterium, and the ISR also can be defined as a NHR. However, how the colonization signal is and how systemic resistance to pathogens is developed is still unclear. In this study, we demonstrated that the extracellular polysaccharides (EPSs) of Bacillus cereus AR156 could act as novel microbe-associated molecular patterns (MAMPs) and function in the early perception status of the ISR of B. cereus AR156. The results revealed that B. cereus AR156 EPS could induce systemic resistance to Pst DC3000 in Arabidopsis. Cellular defense response markers such as hydrogen peroxide accumulation, callose deposition, and defense-associated enzyme were induced upon challenge inoculation in the leaves primed by EPS. Moreover, the defense-related genes PR1, PR2, and PR5 and mitogen-activated kinases (MAPK) cascade marker gene MPK6 were concurrently expressed in the leaves of EPS-treated plants and induced higher resistance to Pst DC3000 in Col-0 than that in the jar1 or etr1 mutants. The protection was absent in the NahG transgenic plants and npr1 mutant, suggesting an activation of the salicylic acid (SA)- and the MAPK-dependent signaling pathways with NPR1-dependent by B. cereus AR156 EPS. In conclusion, B. cereus AR156 EPS play an important role in MAMP perception during the process of rhizobacteria-triggered NHR. This study is the first to illustrate how AR156 induces systemic resistance to Pst DC3000 in Arabidopsis. It also provides the first explanation of how plants perceive colonization of non-pathogenic bacteria and how rhizobacteria trigger ISR to plant pathogens.

Highlights

  • Plant growth is influenced by a variety of biotic and abiotic factors

  • D, B. cereus AR156 Extracellular polysaccharides (EPS) could enhance the expression level of MPK6 at 1 dpt, and in the leaves of Arabidopsis ecotype Col-0, which was treated with B. cereus AR156 EPS and inoculated with Pst Pseudomonas syringae pv. tomato DC3000 (DC3000), the expression level of MPK6 reached a maximum at 6 hpi (Figure 7C); in the leaves of plants inoculated with Pst DC3000 alone, the expression level of MPK6 reached a maximum at 12 hpi (Figure 7C). These results suggest that B. cereus AR156 EPS could be microbe-associated molecular patterns (MAMPs) and trigger induced systemic response (ISR) through Mitogen-activated protein kinases (MAPK) signaling as well, and the activation of MAPK signaling in plants, pre-treated with B. cereus AR156 EPS and inoculated with Pst DC3000 show more faster and rapid than that in plants inoculated with Pst DC3000 alone

  • Series of studies have established the functions of beneficial plant growth promotion rhizobacteria (PGPRs) on improving plant health by increasing resistance to insect pests, FIGURE 7 | The EPSs of B. cereus AR156 induced MAPK6 expression in the leaves of Arabidopsis ecotype Col-0 plants upon Pst DC3000 attack

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Summary

Introduction

To survive from an antagonistic and complex environment, the plant has evolved a series of inducible defense mechanisms, which can assist them to activate appropriate defense reactions upon pathogen invasion (Niu et al, 2011; Jiang et al, 2015). Well-researched examples of plant-induced resistance include SAR and rhizobacteria-ISR, which are phenotypically similar to each other and both of them can be defined as a non-host resistance (NHR) (Conrath et al, 2002; Jiang et al, 2015). ISR requires the JA and ET signaling pathways (Van Loon et al, 1998; Jiang et al, 2015) and is combined with the high expression of the plant defensin 1.2 (PDF1.2) (Van Oosten et al, 2008; Jiang et al, 2015)

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