Plant growth-promoting rhizobacterium Bacillus cereus AR156 - induced
systemic resistance against multiple pathogens by priming of phytoalexin
synthesis and secretion
Phytoalexin plays an important role in plant immunity. However, the
mechanism of how phytoalexin is induced by beneficial microorganisms
against broad-spectrum pathogens remains elusive. This study showed that
B. cereus AR156 could trigger ISR against broad-spectrum disease.
RNA-seq and camalexin content assays showed that AR156-triggered ISR can
induce the accumulation of phytoalexin such as camalexin synthesis and
secretion-related genes. Moreover, it was found that AR156-triggered ISR
elevates camalexin accumulation by increasing the expression of
camalexin synthesis genes upon pathogen infection. Further studies
revealed that WRKY33 was required for the induction of camalexin
accumulation by AR156 during the pathogen infection. Compared to the
control inoculated with Phytophthora capsici and Botrytis
cinerea only, the biomass of P. capsici and B. cinerea in
AR156 pretreated wrky33 mutant plants were quite similar.
AR156-induced ISR resistance to Pseudomonas syringae pv.
tomato DC3000 ( Pst DC3000) was significantly attenuated
in the wrky33 mutant. Furthermore, the study reveals that AR156
could up-regulate the expression level of PEN3 and PDR12,
which act as camalexin transporter. In addition, we found that PEN3 and
PDR12 served as positive regulators involved in AR156-triggered ISR
against pathogens. Specifically, PEN3 and PDR12 participated in
AR156-triggered ISR against fungi and oomycetes, while PEN3 was involved
in AR156-triggered ISR against Pst DC3000. In summary, B.
cereus AR156 triggered induced systemic resistance against B.
cinerea, Pst DC3000 and P. capsici by priming of
phytoalexin synthesis and secretion. Our study first proposed that the
WRKY33 as a core factor is involved in regulating AR156-induced
accumulation and secretion of phytoalexin, and we deeply elucidated the
mechanism of AR156-induced phytotoxin accumulation resistance to