computational prediction and molecular characterization of an oomycete effector and the cognate arabidopsis resistance gene计算预测和分子特性的oomycete效应和同源拟南芥耐药基因.pdfVIP

computational prediction and molecular characterization of an oomycete effector and the cognate arabidopsis resistance gene计算预测和分子特性的oomycete效应和同源拟南芥耐药基因.pdf

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computational prediction and molecular characterization of an oomycete effector and the cognate arabidopsis resistance gene计算预测和分子特性的oomycete效应和同源拟南芥耐药基因

Computational Prediction and Molecular Characterization of an Oomycete Effector and the Cognate Arabidopsis Resistance Gene ¤ Sandra Goritschnig, Ksenia V. Krasileva , Douglas Dahlbeck, Brian J. Staskawicz* Department of Plant and Microbial Biology, University of California Berkeley, Berkeley, California, United States of America Abstract Hyaloperonospora arabidopsidis (Hpa) is an obligate biotroph oomycete pathogen of the model plant Arabidopsis thaliana and contains a large set of effector proteins that are translocated to the host to exert virulence functions or trigger immune responses. These effectors are characterized by conserved amino-terminal translocation sequences and highly divergent carboxyl-terminal functional domains. The availability of the Hpa genome sequence allowed the computational prediction of effectors and the development of effector delivery systems enabled validation of the predicted effectors in Arabidopsis. In this study, we identified a novel effector ATR39-1 by computational methods, which was found to trigger a resistance response in the Arabidopsis ecotype Weiningen (Wei-0). The allelic variant of this effector, ATR39-2, is not recognized, and two amino acid residues were identified and shown to be critical for this loss of recognition. The resistance protein responsible for recognition of the ATR39-1 effector in Arabidopsis is RPP39 and was identified by map-based cloning. RPP39 is a member of the CC-NBS-LRR family of resistance proteins and requires the signaling gene NDR1 for full activity. Recognition of ATR39-1 in Wei-0 does not inhibit growth of Hpa strains expressing the effector, suggesting complex mechanisms of pathogen evasion of recognition, and is similar to what has been shown in several oth

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