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Impaired sterol ester synthesis alters the response of Arabidopsis thaliana to Phytophthora infestans
Author(s) -
Kopischke Michaela,
Westphal Lore,
Schneeberger Korbinian,
Clark Richard,
Ossowski Stephan,
Wewer Vera,
Fuchs René,
Landtag Jörn,
Hause Gerd,
Dörmann Peter,
Lipka Volker,
Weigel Detlef,
SchulzeLefert Paul,
Scheel Dierk,
Rosahl Sabine
Publication year - 2013
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1111/tpj.12046
Subject(s) - phytophthora infestans , callose , biology , arabidopsis thaliana , pathosystem , sterol , arabidopsis , mutant , biochemistry , botany , gene , cholesterol
Summary 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 PEN 2. 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. ERP 1 encodes a phospholipid:sterol acyltransferase ( PSAT 1) that catalyzes the formation of sterol esters. Consistent with this, the tested T‐ DNA insertion lines of PSAT 1 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 PMR 4/ GSL 5 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.