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Consonni, C.* ; Humphry, M.E.* ; Hartmann, H.A.* ; Livaja, M. ; Durner, J. ; Westphal, L.* ; Vogel, J.* ; Lipka, V.* ; Kemmerling, B.* ; Schulze-Lefert, P.* ; Somerville, S.C.* ; Panstruga, R.*

Conserved requirement for a plant host cell protein in powdery mildew pathogenesis.

Nat. Genet. 38, 716-720 (2006)
DOI
Open Access Green as soon as Postprint is submitted to ZB.
In the fungal phylum Ascomycota, the ability to cause disease in plants and animals has been 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 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 dicotyledonous plant species Arabidopsis thaliana. Epistasis analysis showed that mlo resistance in A. thaliana does not involve the signaling molecules ethylene, jasmonic acid or salicylic acid, but requires a syntaxin, glycosyl hydrolase and ABC transporter. 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 (powdery mildews) the ability to cause disease has been a stable trait throughout phylogenesis. © 2006 Nature Publishing Group.
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Publication type Article: Journal article
Document type Scientific Article
Corresponding Author
ISSN (print) / ISBN 1061-4036
e-ISSN 1546-1718
Journal Nature Genetics
Quellenangaben Volume: 38, Issue: 6, Pages: 716-720 Article Number: , Supplement: ,
Publisher Nature Publishing Group
Publishing Place New York, NY
Non-patent literature Publications
Reviewing status Peer reviewed