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Title: CONSERVED REQUIREMENT FOR A PLANT HOST CELL PROTEIN IN POWDERY MILDEW PATHOGENESIS

Author
item CONSONNI, CHIARA - MAX PLANCK-PLANT BREEDING
item HUMPHRY, MATTHEW - CARNEGIE INSTITUTION
item HARTMANN, ANDREAS - MAX PLANCK-PLANT BREEDING
item LIVAJA, MAREN - GSF-CTR ENVIRONMENT/HEALT
item DURNER, JORG - GSF-CTR ENVIRONMENT/HEALT
item WESTPHAL, LORE - INST-PLANT BIOCHEMISTRY
item Vogel, John
item LIPKA, VOLKER - EBERHARD-KARLS UNIV
item KEMMERLING, BIRGIT - EBERHARD-KARLS UNIV
item SCHULZE, LEFERT - MAX PLANCK-PLANT BREEDING
item SOMERVILLE, SHAUNA - CARNEGIE INSTITUTION
item PANSTRUGA, RALPH - MAX PLANCK-PLANT BREEDING

Submitted to: Nature Genetics
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 4/24/2006
Publication Date: 5/28/2006
Citation: Consonni, C., Humphry, M., Hartmann, A., Livaja, M., Durner, J., Westphal, L., Vogel, J.P., Lipka, V., Kemmerling, B., Schulze, L., Somerville, S., Panstruga, R. 2006. Conserved requirement for a plant host cell protein in powdery mildew pathogenesis. Nature Genetics. 38:716-720.

Interpretive Summary: This paper describes the cloning and characterization of three partially functionally redundant Arabidopsis genes, Atmlo2, Atmlo6, Atmlo12, that are co-orthologs of barley Mlo. Mutations in the AtMLO genes result in powdery mildew resistance that is not dependent on the signaling through known defense pathways. Atmlo-mediated resistance does require a syntaxin, a glycosyl hydrolase and an ABC transporter. In Arabidopsis Atmlo mutants defective in salicylic acid signaling, resistance could be uncoupled from undesired pleiotropic phenotypes previously thought to be inevitably linked with mlo immunity. These findings imply that a common host cell entry mechanism of powdery mildew fungi evolved once and at least 200 million years ago, suggesting that within the Erysiphales, comprising ~500 powdery mildew species, the ability to cause disease has been a stable trait throughout evolution.

Technical Abstract: In the fungal phylum Ascomycota, the ability to cause disease in plants and animals was gained and lost repeatedly during phylogenesis. In monocotyledonous barley, loss-of-function mlo alleles result in effective immunity against the Ascomycete, Blumeria graminis f. sp. hordei, the causal agent of the powdery mildew disease. However, mlo-based disease resistance has been considered a barley-specific phenomenon to date. Here, we demonstrate a conserved requirement for MLO proteins in powdery mildew pathogenesis in the distantly related dicotyledonous plant species, Arabidopsis thaliana. Loss-of-function alleles of three partially functionally redundant AtMLO co-orthologs of barley Mlo confer resistance to two powdery mildew species. Epistasis analysis revealed that mlo resistance in Arabidopsis does not entail signaling molecules ethylene, jasmonic acid or salicylic acid, but requires a syntaxin, glycosyl hydrolase and ABC transporter. In Arabidopsis mlo mutants defective in salicylic acid signaling, resistance could be uncoupled from undesired pleiotropic phenotypes previously thought to be inevitably linked with mlo immunity. These findings imply that a common host cell entry mechanism of powdery mildew fungi evolved once and at least 200 million years ago, suggesting that within the Erysiphales, comprising ~500 powdery mildew species, the ability to cause disease has been a stable trait throughout phylogenesis.