Oomycete effector AVRblb2 targets cyclic nucleotide-gated channels through calcium sensors to suppress pattern-triggered immunity

Abstract

SUMMARYTransient, rapid increase of cytosolic Ca2+upon pathogen infection is essential for plant pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI). Several cyclic nucleotide-gated channels (CNGCs) have been implicated; however, their regulatory mechanisms remain elusive. Here, thePhytophthora infestansRXLR effector AVRblb2 family targeted NbCNGC18–20 at the plasma membrane, inhibiting Ca2+influx and PTI. AVRblb2 required calmodulin (CaM) and calmodulin-like (CML) proteins as co-factors to interact withN. benthamianaCNGCs (NbCNGCs), forming the AVRblb2-CaM/CML-NbCNGCs complex. After recognizing PAMPs, NbCNGC18 formed active heteromeric channels with other CNGCs, potentially providing selectivity for diverse signals to fine-tune cytosolic Ca2+levels and responses. AVRblb2 suppressed the Ca2+influx and oxidative burst induced by NbCNGC18 heteromeric complexes. Silencing CNGC18, CNGC20, and CNGC25 compromised the effect of AVRblb2 onP. infestansvirulence, confirming that AVRblb2 contributed to virulence by targeting CNGCs. Our findings delineated the regulatory mechanism and role of effector-targeted Ca2+channels in plant innate immunity.