Abstract

We have previously reported a phenomenon of “conditional pathogenesis”, in which, a drought-tolerant rhizobacterium, Pseudomonas putida AKMP7, promotes plant growth under well-watered conditions, while, deteriorating plant health under water-stressed conditions, in Arabidopsis thaliana seedlings. To understand the molecular mechanisms behind this phenomenon, we studied the modulation of salicylic acid (SA) biosynthesis as well as SA-responsive gene expression, involved in systemic acquired resistance (SAR), in A. thaliana, by AKMP7, under well-watered and water-stressed conditions. We found that, the plant SA levels were upregulated by AKMP7, both under, well-watered as well as water-stressed conditions. However, the SA signaling gene, Non-expressor of Pathogenesis Related gene 1 (NPR1) and Pathogenesis Related gene 1 (PR1) were upregulated under well-watered conditions and suppressed under water-stress, in AKMP7 inoculated seedlings. To understand the reason for this, we studied the expression of NPR4, a negative regulator of NPR1, and, NPR3, a negative regulator of PR1. We observed that, AKMP7 suppresses NPR1 and, consequently, PR1 genes, by upregulating NPR4 under water stress. To understand the potential role of NPR4 in conditional-pathogenesis, we performed physiological studies with NPR4 knockout mutants of A. thaliana and found that the NPR4 mutants did not exhibit any signs of the characteristic growth retardation caused by AKMP7 inoculation, under water stress. Preliminary studies with the model pathogen, Pseudomonas syringae, indicate that AKMP7 may lead to enhanced disease suppression under well-watered conditions, but not under water-stress. Taken together, our data suggest that, AKMP7 causes conditional pathogenesis by an overall compromise in plant immune response under water-stress.

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