The effector AGLIP1 hijacks peroxidase OsAPX8 to coordinate rice immune suppression and ROS-Driven cell death for...

Necrotrophic fungi such as Rhizoctonia solani, the causal agent of rice sheath blight (RSB), release effectors that suppress host immune defenses and trigger host cell death. However, the molecular basis for this dual functionality remains poorly understood.

This study aimed to characterize the effector AGLIP1 from R. solani, elucidate its dual role in modulating rice immune responses and cell death, and investigate the molecular mechanism by which it promotes infection.

We combined transgenic over-expression lines, CRISPR-Cas9 knockouts, host-induced gene-silenced (HIGS) plants, pathogenesis assays, interaction proteomics, enzyme-kinetics measurements, and confocal imaging to dissect AGLIP1 activity and its impact on OsAPX8.

We showed the effector AGLIP1 from R. solani, and reveal that it simultaneously dampens basal immune responses and triggers reactive oxygen species (ROS)-mediated cell death in rice. Functional assays demonstrated that AGLIP1 expression in rice cells suppresses defense-associated gene expression and leads to excessive ROS accumulation. Consistently, HIGS of AGLIP1 significantly enhanced rice resistance to sheath blight, confirming that AGLIP1 is a crucial virulence factor. Furthermore, AGLIP1 physically interacts with the rice ascorbate peroxidase OsAPX8, a chloroplast-targeted enzyme which positively regulates RSB resistance. AGLIP1 binding inhibits the peroxidase activity of OsAPX8 and relocalizes this enzyme from chloroplasts to peroxisomes, compromising the host's ROS-scavenging defenses. Moreover, overexpression of OsAPX8 in plant cells attenuates AGLIP1-induced cell death, supporting the notion that AGLIP1 promotes cell death by inactivating and misdirecting OsAPX8.

Our findings uncover a novel virulence mechanism utilized by R. solani, where the effector AGLIP1 subverts host antioxidant defenses via OsAPX8 inhibition and mislocalization, facilitating pathogen infection. This insight highlights potential breeding targets, suggesting strategies to stabilize OsAPX8 function or prevent its subversion by AGLIP1 for developing rice cultivars with improved resistance to sheath blight.