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Analysis of Verticillium longisporum-induced gene expression in Arabidopsis thaliana

Subject Area Organismic Interactions, Chemical Ecology and Microbiomes of Plant Systems
Term from 2004 to 2012
Project identifier Deutsche Forschungsgemeinschaft (DFG) - Project number 5471048
 
Final Report Year 2012

Final Report Abstract

Verticillium longisporum is a soil-borne vascular pathogen that causes reduced shoot growth and early senescence in Arabidopsis thaliana. Here we report that these disease symptoms are less pronounced in plants, which lack the receptor of the plant defense hormone jasmonic acid (JA), CORONATINE INSENSITIVE 1 (COI1). The number of plants with microsclerotia, which are detected at late stages of the disease on dead plant material, was reduced in coi1, indicating that completion of the fungal life cycle is impaired. Initial colonization of the roots was comparable in wild-type and coi1 plants as detected by laser scan microscopy of a GFP- tagged Verticillium strain. Consistently, fungal DNA accumulated to similar levels in petioles of wild-type and coi1 plants at 10 days post infection (dpi). Contrary to the expectation that the hormone receptor mutant coi1 should display the same phenotype as the corresponding hormone biosynthesis mutant dde2, dde2 plants developed wild-type-like disease symptoms. Marker genes of the JA or JA/ethylene defense pathway were induced in petioles of wild-type but not in petioles of dde2 plants indicating that fungal compounds that would activate the known COI1-dependent defense processes were absent. Grafting experiments revealed that the susceptibility-enhancing COI1 function acts in the roots. In combination with the previously reported results on the Fusarium oxysporum/Arabidopsis interaction, this study points at a conserved strategy of these two vascular pathogens to weaken the host tissue by activating an unknown COI1-dependent mechanism in the roots which influences diseasepromoting processes in the shoot. Microarray analysis has identified 1219 genes that are upregulated in petioles of wild-type plants at 15 dpi. Many of them are also up-regulated by infection with biotrophic pathogens through the SA pathway. However, mutants defective in either SA accumulation or SA synthesis are not more susceptible indicating that the defense response is not efficient.

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