New papers from the Hückelhoven, Schwab, Isono and Gietl labs.
Genetic loss of susceptibility: a costly route to disease resistance?
Ralph Hückelhoven, Ruth Eichmann, Corina Weis, Caroline Hoefle and Reinhard K. Proels (2013).
Plant Pathology
The susceptibility of plants to microbial pathogens involves molecular interactions between microbial effectors and host targets. In most cases, pathogen effectors prevent recognition or suppress host defence. However, successful suppression of host defence is not always sufficient for pathogenesis, which requires further host components that meet the demands of pathogen development and nutrition. Additionally, the plants possess negative regulators of immune response to avoid autoimmunity and unnecessary investment into defence in environments with little disease pressure. Consequently, disease susceptibility can be lost by mutation of negative regulators of defence, but also of other host factors that otherwise support the successful pathogen. Here, genetic loss of susceptibility to adapted microbial patho- gens is reviewed, with a focus on examples of lost susceptibility to powdery mildew. Costs of resistance and potential consequences for application in breeding and biotechnology are discussed.
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CYP83A1 is required for metabolic compatibility of Arabidopsis with the adapted powdery mildew fungus Erysiphe cruciferarum.
Corina Weis, Ulrich Hildebrandt, Thomas Hoffmann, Christoph Hemetsberger, Sebastian Pfeilmeier, Constanze König, Wilfried Schwab, Ruth Eichmann and Ralph Hückelhoven (2014).
New Phytologist
_ Aliphatic glucosinolates function in the chemical defense of Capparales. The cytochrome P450 83A1 monooxygenase (CYP83A1) catalyzes the initial conversion of methionine- derived aldoximes to thiohydroximates in the biosynthesis of glucosinolates, and thus cyp83a1 mutants have reduced levels of aliphatic glucosinolates.
_ Loss of CYP83A1 function leads to dramatically reduced parasitic growth of the biotrophic powdery mildew fungus Erysiphe cruciferarum on Arabidopsis thaliana. The cyp83a1 mutants support less well the germination and appressorium formation of E. cruciferarum on the leaf surface and post-penetration conidiophore formation by the fungus. By contrast, a myb28-1 myb29-1 double mutant, which totally lacks aliphatic glucosinolates, shows a wild- type level of susceptibility to E. cruciferarum.
_ The cyp83a1 mutants also lack very-long-chain aldehydes on their leaf surface. Such alde- hydes support appressorium formation by E. cruciferarum in vitro. In addition, when chemi- cally complemented with the C26 aldehyde n-hexacosanal, cyp83a1 mutants can again support appressorium formation. The mutants further accumulate 5-meth- ylthiopentanaldoxime, the potentially toxic substrate of CYP83A1.
_ Lossofpowderymildewsusceptibilitybycyp83a1maybeexplainedbyareducedsupplyof the fungus with inductive signals from the host and an accumulation of potentially fungitoxic metabolites.
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Endoplasmic reticulum KDEL-tailed cysteine endopeptidase 1 of Arabidopsis (AtCEP1) is involved in pathogen defense.
Timo Höwing, Christina Huesmann, Caroline Hoefle, Marie-Kristin Nagel, Erika Isono, Ralph Hückelhoven and Christine Gietl (2014).
Programmed cell death (PCD) is a genetically determined process in all multicellular organisms. Plant PCD is effected by a unique group of papain-type cysteine endopeptidases (CysEP) with a C-terminal KDEL endoplasmic reticulum (ER) retention signal (KDEL CysEP). KDEL CysEPs can be stored as pro-enzymes in ER-derived endomembrane compartments and are released as mature CysEPs in the final stages of organelle disintegration. KDEL CysEPs accept a wide variety of amino acids at the active site, including the glycosylated hydroxyprolines of the extensins that form the basic scaffold of the cell wall. In Arabidopsis, three KDEL CysEPs (AtCEP1, AtCEP2, and AtCEP3) are expressed. Cell- and tissue-specific activities of these three genes suggest that KDEL CysEPs participate in the abscission of flower organs and in the collapse of tissues in the final stage of PCD as well as in developmental tissue remodeling. We observed that AtCEP1 is expressed in response to biotic stress stimuli in the leaf. atcep1 knockout mutants showed enhanced susceptibility to powdery mildew caused by the biotrophic ascomycete Erysiphe cruciferarum. A translational fusion protein of AtCEP1 with a three-fold hemaglutinin-tag and the green fluorescent protein under control of the endogenous AtCEP1 promoter (PCEP1::pre-pro-3xHA-EGFP-AtCEP1-KDEL) rescued the pathogenesis phenotype demonstrating the function of AtCEP1 in restriction of powdery mildew. The spatiotemporal AtCEP1-reporter expression during fungal infection together with microscopic inspection of the interaction phenotype suggested a function of AtCEP1 in controlling late stages of compatible interaction including late epidermal cell death. Additionally, expression of stress response genes appeared to be deregulated in the interaction of atcep1 mutants and E. cruciferarum. Possible functions of AtCEP1 in restricting parasitic success of the obligate biotrophic powdery mildew fungus are discussed.
