February
2015
, Volume
28
, Number
2
Pages
122
-
133
Authors
Katrin Geissler,1
Lennart Eschen-Lippold,1
Kai Naumann,1
Korbinian Schneeberger,2
Detlef Weigel,2
Dierk Scheel,1
Sabine Rosahl,1 and
Lore Westphal1
Affiliations
1Department of Stress and Developmental Biology, Leibniz Institute of Plant Biochemistry, Weinberg 3, D-06120 Halle (Saale), Germany; 2Department of Molecular Biology, Max Planck Institute for Developmental Biology, D-72076 Tübingen, Germany
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Accepted 20 October 2014.
Abstract
Mechanistically, nonhost resistance of Arabidopsis thaliana against the oomycete Phytophthora infestans is not well understood. Besides PEN2 and PEN3, which contribute to penetration resistance, no further components have been identified so far. In an ethylmethane sulphonate–mutant screen, we mutagenized pen2-1 and screened for mutants with an altered response to infection by P. infestans. One of the mutants obtained, enhanced response to Phytophthora infestans6 (erp6), was analyzed. Whole-genome sequencing of erp6 revealed a single nucleotide polymorphism in the coding region of the kinase domain of At1g08720, which encodes the putative MAPKKK ENHANCED DISEASE RESISTANCE1 (EDR1). We demonstrate that three independent lines with knock-out alleles of edr1 mount an enhanced response to P. infestans inoculation, mediated by increased salicylic acid signaling and callose deposition. Moreover, we show that the single amino acid substitution in erp6 causes the loss of in vitro autophosphorylation activity of EDR1. Furthermore, growth inhibition experiments suggest a so-far-unknown involvement of EDR1 in the response to the pathogen-associated molecular patterns flg22 and elf18. We conclude that EDR1 contributes to the defense response of A. thaliana against P. infestans. Our data position EDR1 as a negative regulator in postinvasive nonhost resistance.
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© 2015 The American Phytopathological Society