Kopischke, M.; Westphal, L.; Schneeberger, K.; Clark, R.; Ossowski, S.; Wewer, V.; Fuchs, R.; Landtag, J.; Hause, G.; Dörmann, P.; Lipka, V.; Weigel, D.; Schulze-Lefert, P.; Scheel, D.; Rosahl, S. Impaired sterol ester synthesis alters the response of Arabidopsis thaliana to Phytophthora infestans Plant J 73, 456-468, (2013) DOI: 10.1111/tpj.12046
Non-host resistance of Arabidopsis thaliana against Phytophthora infestans, the causal agent of late blight disease of potato, depends on efficient extracellular pre- and post-invasive resistance responses. Pre-invasive resistance against P. infestans requires the myrosinase PEN2. To identify additional genes involved in non-host resistance to P. infestans, a genetic screen was performed by re-mutagenesis of pen2 plants. Fourteen independent mutants were isolated that displayed an enhanced response to Phytophthora (erp) phenotype. Upon inoculation with P. infestans, two mutants, pen2-1 erp1-3 and pen2-1 erp1-4, showed an enhanced rate of mesophyll cell death and produced excessive callose deposits in the mesophyll cell layer. ERP1 encodes a phospholipid:sterol acyltransferase (PSAT1) that catalyzes the formation of sterol esters. Consistent with this, the tested T-DNA insertion lines of PSAT1 are phenocopies of erp1 plants. Sterol ester levels are highly reduced in all erp1/psat1 mutants, whereas sterol glycoside levels are increased twofold. Excessive callose deposition occurred independently of PMR4/GSL5 activity, a known pathogen-inducible callose synthase. A similar formation of aberrant callose deposits was triggered by the inoculation of erp1 psat1 plants with powdery mildew. These results suggest a role for sterol conjugates in cell non-autonomous defense responses against invasive filamentous pathogens.
Eschen-Lippold, L.; Landgraf, R.; Smolka, U.; Schulze, S.; Heilmann, M.; Heilmann, I.; Hause, G.; Rosahl, S. Activation of defense against Phytophthora infestans in potato by down-regulation of syntaxin gene expression New Phytol 193, 985-996, (2012) DOI: 10.1111/j.1469-8137.2011.04024.x
The oomycete Phytophthora infestans is the
causal agent of late blight, the most devastating disease of potato. The
importance of vesicle fusion processes and callose deposition for
defense of potato against Phytophthora infestans was analyzed.Transgenic plants were generated, which express RNA interference
constructs targeted against plasma membrane‐localized SYNTAXIN‐RELATED 1
(StSYR1) and SOLUBLE N‐ETHYLMALEIMIDE‐SENSITIVE FACTOR ADAPTOR PROTEIN
33 (StSNAP33), the potato homologs of Arabidopsis AtSYP121 and AtSNAP33,
respectively.Phenotypically, transgenic plants grew normally, but
showed spontaneous necrosis and chlorosis formation at later stages. In
response to infection with Phytophthora infestans, increased resistance
of StSYR1‐RNAi plants, but not StSNAP33‐RNAi plants, was observed. This
increased resistance correlated with the constitutive accumulation of
salicylic acid and PR1 transcripts. Aberrant callose deposition in
Phytophthora infestans‐infected StSYR1‐RNAi plants coincided with
decreased papilla formation at penetration sites. Resistance against the
necrotrophic fungus Botrytis cinerea was not significantly altered.
Infiltration experiments with bacterial solutions of Agrobacterium
tumefaciens and Escherichia coli revealed a hypersensitive phenotype of
both types of RNAi lines.The enhanced defense status and the reduced
growth of Phytophthora infestans on StSYR1‐RNAi plants suggest an
involvement of syntaxins in secretory defense responses of potato and,
in particular, in the formation of callose‐containing papillae.
Bethke, G.; Unthan, T.; Uhrig, J. F.; Pöschl, Y.; Gust, A. A.; Scheel, D.; Lee, J. Flg22 regulates the release of an ethylene
response factor substrate from MAP kinase 6 in Arabidopsis thaliana via
ethylene signaling Proc Natl Acad Sci USA 106, 8067-72, (2009) DOI: 10.1073/pnas.0810206106
Mitogen-activated protein kinase (MAPK)mediated responses are in part regulated by the repertoire of MAPK substrates, which is still poorly elucidated in plants. Here, the in vivo enzymesubstrate interaction of the Arabidopsis thaliana MAP kinase, MPK6, with an ethylene response factor (ERF104) is shown by fluorescence resonance energy transfer. The interaction was rapidly lost in response to flagellin-derived flg22 peptide. This complex disruption requires not only MPK6 activity, which also affects ERF104 stability via phosphorylation, but also ethylene signaling. The latter points to a novel role of ethylene in substrate release, presumably allowing the liberated ERF104 to access target genes. Microarray data show enrichment of GCC motifs in the promoters of ERF104up-regulated genes, many of which are stress related. ERF104 is a vital regulator of basal immunity, as altered expression in both erf104 and overexpressors led to more growth inhibition by flg22 and enhanced susceptibility to a non-adapted bacterial pathogen.