Assistant Professor Auburn University Auburn, Alabama
Body of Abstract: In plants, trade-offs between growth and defense have appeared as a major pitfall in genetically engineering/improving defense capacity. To understand if and/or how plants could coordinate growth and defense responses, we here exploit the role and mode of plant growth-promoting rhizobacteria (PGPR)-mediated ‘induced systemic resistance (ISR)’, a phenomenon capable of priming a broad-spectrum disease resistance without the usually accompanied growth penalty. Here, we i) Screened and isolated the ISR-inducible PGPR strains, Bacillus subtilis and Pseudomonas oryzahabitans, as well as a negative PGPR strain, Paenibacillus polymyxa. and ii) Surveyed the expression of different PGPR-responsive genes to delineate the circuitry of hormone, such as jasmonate and salicylic acid (SA), signal transductions in local and systemic tissues during ISR activations. When plant roots were inoculated with B. subtilis and P. oryzahabitans, they induced jasmonate, but not SA, biosynthesis, and in turn activated jasmonate, both 12-oxophytodienoic acid (OPDA) and jasmonate-isoleucine (JA-Ile), signaling. The local defense then conveyed a mobile, long-distance signal to systemic leaf tissues where it can activate OPDA signaling, but not produce JA nor activate JA-Ile signaling, suggesting that a ISR signal is OPDA or its precursor. On the other hand, both inoculated and naïve tissues upregulated the expression of Pathogenesis-related Protein (PR) 1 and 4, molecular markers for SA signaling, although they could not stimulate SA biosynthesis, indicating that ISR requires SA-independent PR1 gene pathways. In line with this scenario, OPDA application can directly induce the accumulation of PR1 transcripts without affecting the cellular level of SA. Together, we propose that ISR requires in local tissues the accumulation of OPDA that move to systemic tissues where activate OPDA response defense gene and SA-independent PR1 gene pathways.