Unknown,Transcriptomics,Genomics,Proteomics

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Systemic responses to Pseudomonas syringae infection

ABSTRACT: We used three different strains of Pseudomonas syringae pv tomato DC3000 to investigate systemic responses to infection in Arabidopsis and the development of SAR. Wildtype DC3000, the hrpA mutant and DC3000 carrying the avirulence gene avrRpm1 were syringe infiltrated into 4-week-old plants at a concentration of 10e8 cfu/ml. At least 5 leaves per plant were infiltrated and at least 10 plants were pooled for each sample. Systemic, uninfected tissue was then harvested at 8, 12 and 21h after inoculation. Three independent experiments were carried out to give three biological replicates for each timepoint. 27 samples were used in this experiment.

ORGANISM(S): Arabidopsis thaliana

SUBMITTER: William Truman

PROVIDER: E-GEOD-19264 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Plant 9-lipoxygenases (9-LOX) and α-dioxygenases (α-DOX) initiate the synthesis of oxylipins after bacterial infection. Here, the role of these enzymes in plant’s defense was investigated using individual Arabidopsis thaliana lox1 and dox1 mutants and a double lox1 dox1 mutant. Studies with Pseudomonas syringae pv tomato (Pst) revealed the enhanced susceptibility of lox1 to the virulent strain Pst DC3000 and the partial impairment of lox1 and dox1 mutants to activate systemic acquired resistance. Notably, both defects were enhanced in the lox1 dox1 plants as compared with individual mutants. We found that pre-treatment with 9-LOX- and -DOX-generated oxylipins protected plant tissues against bacterial infection. The strongest effect in this respect was exerted by 9-ketooctadecatrienoic acid (9-KOT), which is produced from linolenic acid by 9-LOX. Quantification of 9-KOT revealed its accumulation after bacterial infection. The levels were reduced in lox1 and lox1 dox1 plants but strongly increased in the dox1 mutant due to metabolic interaction of the two pathways. Transcriptional analyses indicated that 9-KOT pre-treatment modifies hormone homeostasis during bacterial infection. The nature of the changes detected suggested that 9-KOT interfers the hormonal changes caused by bacterial effectors. This notion was substantiated by the finding that 9-KOT failed to reduce the growth of PstDC3000hrpA, a mutant compromised in effector secretion, and of the avirulent strain Pst DC3000 avrRpm1. Further support to the action of the 9-LOX- and -DOX-oxylipin pathways as modulators of hormone homeostasis was the observation that lox1 dox1 seedlings are hypersensitive to the growth-inhibitory effect of ABA and showed enhanced activation of ABA-inducible marker genes. Two experiments, Col-0 treated with 9-KOT vs. Col-0 treated with water and Col-0 treated with 9-KOT vs. Col-0 treated with water after treatment with Pst DC3000. Biological replicates: 4 control replicates treated , 4 9-KOT treated replicates; 4 control treated and Pst DC3000 replicates and 4 9-KOT treated and Pst DC3000 replicates

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Systemic responses to Pseudomonas syringae infection

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