An oomycete effector targets host calmodulin to suppress plant immunity.

Tropical and subtropical fruit trees face serious threats of oomycete-caused plant diseases. However, the molecular mechanism by which oomycete pathogens suppress the immunity of these fruit trees remains largely unclear. Effectors play a crucial role in the pathogenesis of plant pathogenic oomycetes. Here, we found that a conserved RXLR-type effector protein PlAvh222 from the pathogen Peronophythora litchii is required for its full virulence on litchi. Expression of PlAvh222 in Nicotiana benthamiana leaves suppressed INF1-induced immune responses and promoted Phytophthora capsici infection. Further research demonstrated that PlAvh222 interacted with litchi calmodulins (LcCaMs) in vivo and in vitro. Silencing of NbCaM1/2/3/4 attenuated the ability of PlAvh222 to enhance N. benthamiana susceptibility. The C-terminal CaM-binding region of PlAvh222 is required for targeting LcCaM and to suppress N. benthamiana immune responses, including programmed cell death (PCD) and reactive oxygen species (ROS) burst. In addition, the interaction between PlAvh222 and LcCaM1/2/3 increases the accumulation of LcCaM1/2/3 and reduces levels of cytosolic Ca ([Ca]). Blocking [Ca] influx leads to compromised PCD in N. benthamiana. Our results reveal that the oomycete effector promotes pathogen infection through suppressing [Ca]-induced plant immunity.