Project description:We sought to compare and contrast plant host and bacterial transcriptional changes during compatible infections that cause disease (albeit within different symptoms). We investigated the infection by the two Pseudomonas syringae sensu lato strains P. syringae pv. syringae B728a (Psy) and P. amygdali pv. tabaci 11528 (Pta) of Nicotiana benthamiana at an early time point post inoculation to understand how a plant host responds to two related bacteria with different infection strategies. Plant and bacterial transcriptomes were analyzed prior to and five hours post inoculation.
Project description:Pathogens target phytohormone signalling pathways to promote disease. Plants deploy salicylic acid (SA) mediated defences against biotrophs. Pathogens antagonise SA immunity by activating jasmonate signalling, e.g. Pseudomonas syringae pv. tomato DC3000 produces coronatine (COR), a jasmonate (JA) mimic. This study found unexpected dynamics between SA, JA and COR and co-operation between JAZ jasmonate repressor proteins during DC3000 infection. JA did not accumulate until late in the infection process and was higher in leaves challenged with coronatine deficient P. syringae or in the more resistant JA receptor mutant coi1. JAZ regulation was complex and coronatine alone was insufficient to sustainably induce JAZs. RNA was extracted from leaves of wild type Col-0 or the jaz5/10 mutant plants from leaves 6, 8, 12 or 16 hours after challenged with Pseudomonas syringae pv. tomato DC3000.
