Premium
A conserved Rx LR effector interacts with host RABA ‐type GTP ases to inhibit vesicle‐mediated secretion of antimicrobial proteins
Author(s) -
Tomczynska Iga,
Stumpe Michael,
Mauch Felix
Publication year - 2018
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.13928
Subject(s) - effector , secretion , host (biology) , microbiology and biotechnology , antimicrobial , chemistry , biology , biochemistry , genetics
Summary Plant pathogens of the oomycete genus Phytophthora produce virulence factors, known as Rx LR effector proteins that are transferred into host cells to suppress disease resistance. Here, we analyse the function of the highly conserved Rx LR 24 effector of Phytophthora brassicae . Rx LR 24 was expressed early in the interaction with Arabidopsis plants and ectopic expression in the host enhanced leaf colonization and zoosporangia formation. Co‐immunoprecipitation (Co‐ IP ) experiments followed by mass spectrometry identified different members of the RABA GTP ase family as putative Rx LR 24 targets. Physical interaction of Rx LR 24 or its homologue from the potato pathogen Phytophthora infestans with different RABA GTP ases of Arabidopsis or potato, respectively, was confirmed by reciprocal Co‐ IP . In line with the function of RABA GTP ases in vesicular secretion, Rx LR 24 co‐localized with RABA 1a to vesicles and the plasma membrane. The effect of Rx LR 24 on the secretory process was analysed with fusion constructs of secreted antimicrobial proteins with a pH ‐sensitive GFP tag. PATHOGENESIS RELATED PROTEIN 1 ( PR ‐1) and DEFENSIN ( PDF 1.2) were efficiently exported in control tissue, whereas in the presence of Rx LR 24 they both accumulated in the endoplasmic reticulum. Together our results imply a virulence function of Rx LR 24 effectors as inhibitors of RABA GTP ase‐mediated vesicular secretion of antimicrobial PR ‐1, PDF 1.2 and possibly other defence‐related compounds.