Unknown,Transcriptomics,Genomics,Proteomics

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Microarray analysis of med14 and wild type (Col-0) infected with the avirulent bacterial pathogen Pst DC3000/avrRpt2

ABSTRACT: The goal of the microarray experiment was to determine the induction kinetics of transcriptome changes and to identify differentially expressed genes in the Arabidopsis mutant med14 and wild type in response to infection of the avirulent bacterial pathogen Pst DC3000/avrRpt2. Results indicated that med14 exhibited slower kinetcis of transcriptional changes than the wild type after Pst DC3000/avrRpt2 infection, and the induction of a large group of defense genes was suppressed in the med14 mutant. Three biological replicates with leaves from 8 plants per sample were collected at 0, 4, 8, and 12 hours after inoculation with the avirulent bacterial pathogen Pst DC3000/avrRpt2. After extraction, RNA concentration was determined on a NanoDrop Spectrophotometer (Thermofisher Scientific, Waltham, MA) and sample quality was assessed using the 2100 Bioanalyzer (Agilent Technologies, Santa Clara, CA). Each replicate was used as one sample for microarray analysis.

ORGANISM(S): Arabidopsis thaliana

SUBMITTER: Jin Yao

PROVIDER: E-GEOD-45212 | 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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Microarray analysis of med14 and wild type (Col-0) infected with the avirulent bacterial pathogen Pst DC3000/avrRpt2

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