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