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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 möglich sobald Postprint bei der ZB eingereicht worden ist.
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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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
ISSN (print) / ISBN 1061-4036
e-ISSN 1546-1718
Zeitschrift Nature Genetics
Quellenangaben Band: 38, Heft: 6, Seiten: 716-720 Artikelnummer: , Supplement: ,
Verlag Nature Publishing Group
Verlagsort New York, NY
Begutachtungsstatus Peer reviewed