Deciphering mechanisms of Bacillus amyloliquefaciens mediated priming of plant growth and defense responses
Abstract: Beneficial bacteria colonizing plant roots are capable of mediating improved plant growth and enhanced defense responses against biotic and abiotic stresses. Such colonization has been suggested to accumulate brassinosteroid (BR) levels but the mechanisms behind this is not yet completely understood. This study confirms that Bacillus amyloliquefaciens UCMB5113 is capable of promoting growth in Arabidopsis thaliana wild type Col-0 and BR deficient det2-1 mutants. These results suggest that Bacillus potentially promotes growth by elevating the endogenous BR levels which further led to the proposal that Bacillus releases a protein interacting with the BR receptor BRI1 triggering BR dependent signaling. This interaction remains to be established since no such protein was identified in the performed immunoprecipitation. Gene expression analysis revealed that Bacillus was only able to mediate primed defense responses as induced systemic resistance (ISR) in Col-0 but not in det2-1 plants upon challenge with the fungal pathogen Alternaria brassicicola. Since certain BR levels are essential in defense responses of plants, it was suggested that Bacillus was not capable of elevating BR to levels high enough to provide protection against A. brassicicola. GUS assays showed systematic expression of BAK1 in leaves of Bacillus treated plants. Further, the expression was observed to relocate to the inoculation site upon pathogen challenge. These findings suggest a role for BAK1 both in root colonization of Bacillus and defense. BRI1 was also shown to be induced by Bacillus and interestingly, also by a suspension of Bacillus cell walls. This reveals that non-viable bacteria can stimulate BRI1 expression, but it remains to be determined whether non-viable bacteria can mediate primed growth and defense as well. Gene expression analysis identified a probable role for ML genes (1,3,5,8) during colonization of Bacillus. However, pre-liminary studies performed on ml3-1 and ml7-1 mutants did not indicate that they have any major role in ISR.
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