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Programmed cell death (PCD) is a prerequisite for successful development and it limits the spread of biotrophic pathogens in a rapid hypersensitive response at the site of infection. KDEL-tailed cysteine endopeptidases (KDEL CysEP) are a subgroup of papain-type cysteine endopeptidases expressed in tissues undergoing PCD. In  Arabidopsis , three KDEL CysEPs ( AtCEP1 ,  AtCEP2 , and  AtCEP3 ) are expressed. We have previously shown that AtCEP1 is a factor of basal resistance to powdery mildew caused by the biotrophic ascomycete  Erysiphe cruciferarum , and is expressed in spatiotemporal association with the late fungal development on  Arabidopsis  leaves. The endoplasmic reticulum-localized proenzyme of AtCEP1 was further visualized at the haustorial complex encased with callose. The  AtCPR5  gene ( CONSTITUTIVE EXPRESSION OF PR GENES 5 ) is a regulator of expression of pathogenesis related genes. Loss of  AtCPR5  leads to spontaneous expression of chlorotic lesions which was associated with enhanced expression of  AtCEP1 . We used the  atcpr5-2  mutant plants and the  atcep1 atcpr5-2  double mutants harboring a non-functional reporter (P CEP1 ::pre-pro-3xHA-EGFP-KDEL) for visualization of  AtCEP1  promoter activity. We found the specific up-regulation of  AtCEP1  in direct neighborhood of spreading leaf lesions thus likely representing cells undergoing PCD. Furthermore, we found a strong resistance of  atcpr5  mutant plants against infection with  E .  cruciferarum . Loss of  AtCEP1  had no obvious influence on the strong resistance of  atcpr5-2  mutant plants against infection with  E .  cruciferarum . However, the area of necrotic leaf lesions associated with  E .  cruciferarum  colonies was significantly larger in  atcpr5-2  as compared to  atcep1 atcpr5-2  double mutant plants. The presence of AtCEP1 thus contributes to AtCPR5-controlled PCD at the sites of powdery mildew infection.

plos one

Involvement of Arabidopsis thaliana endoplasmic reticulum KDEL-tailed cysteine endopeptidase 1 (AtCEP1) in powdery mildew-induced and AtCPR5-controlled cell death