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Rice blast, caused by the fungus Magnaporthe oryzae , poses a severe threat to global rice production. Although numerous M. oryzae effectors have been identified, the molecular mechanisms remain poorly understood. The effector AvrPii triggers ETI upon recognition by NLR receptor Pii and has been shown to target host exocytosis and oxidative metabolic pathways to suppress immunity. Here, we identify AVIN8 ( Av rPii- in teracting protein 8) as a new target of AvrPii. AVIN8 is an ankyrin-repeat (ANK) protein localized to the plasma membrane and nuclear envelope, with sequence similarity to known ANK calcium channels. AVIN8 expression is induced during early M. oryzae infection. Overexpression of AVIN8 enhances blast resistance, whereas its silencing increases susceptibility. AVIN8 promotes chitin-triggered ROS production in a Ca ²⁺ -dependent manner. In contrast, AvrPii impairs Ca ²⁺ influx and chitin-triggered ROS burst. Our findings reveal a virulence strategy in which M. oryzae effector AvrPii hijacks the Ca ²⁺ influx-associated ANK protein AVIN8 to suppress early calcium and PTI signaling in rice.