Abstract
PEN2 was isolated as a gene involved in nonhost resistance of Arabidopsis thaliana against powdery mildews, and it also functions in nonhost resistance against Colletotrichum species. In this study, we identified lic1 mutants (lesion induced by nonadapted Colletotrichum) that failed to maintain nonhost resistance against Colletotrichum. Nonadapted Colletotrichum did not elevate the efficiency of plant invasion in the lic1 mutant, suggesting that lesion development in the lic1 mutant is not due to fungal invasion. Map-based cloning revealed that LIC1 is allelic to NSL1 encoding a protein with a MACPF domain. The lic1 pad4 and lic1 eds16 double mutants reduced lesion formation compared with the lic1 mutant, indicating the involvement of salicylic acid signaling in the lic1 phenotype. Surprisingly, the pen2 mutation also partially suppressed lesion development in the lic1 mutant, suggesting a link between PEN2-mediated antimicrobial response and the MACPF protein in cell death regulation.
