AUTHOR=Höwing Timo , Huesmann Christina , Hoefle Caroline , Nagel Marie-Kristin , Isono Erika , Huckelhoven Ralph , Gietl Christine 

TITLE=Endoplasmic reticulum KDEL-tailed cysteine endopeptidase 1 of Arabidopsis (AtCEP1) is involved in pathogen defense

JOURNAL=Frontiers in Plant Science

VOLUME=5

YEAR=2014

URL=https://www.frontiersin.org/journals/plant-science/articles/10.3389/fpls.2014.00058

DOI=10.3389/fpls.2014.00058

ISSN=1664-462X

ABSTRACT=<p>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 <italic>Arabidopsis</italic>, three KDEL CysEPs (<italic>AtCEP1</italic>, <italic>AtCEP2</italic>, and <italic>AtCEP3</italic>) 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 <italic>AtCEP1</italic> is expressed in response to biotic stress stimuli in the leaf. <italic>atcep1</italic> knockout mutants showed enhanced susceptibility to powdery mildew caused by the biotrophic ascomycete <italic>Erysiphe cruciferarum</italic>. A translational fusion protein of AtCEP1 with a three-fold hemaglutinin-tag and the green fluorescent protein under control of the endogenous AtCEP1 promoter (P<sub>CEP1</sub>::pre-pro-3xHA-EGFP-AtCEP1-KDEL) rescued the pathogenesis phenotype demonstrating the function of AtCEP1 in restriction of powdery mildew. The spatiotemporal <italic>AtCEP1</italic>-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 <italic>atcep1</italic> mutants and <italic>E. cruciferarum</italic>. Possible functions of AtCEP1 in restricting parasitic success of the obligate biotrophic powdery mildew fungus are discussed.</p>