NADPH oxidase-derived reactive oxygen species: key signaling molecules that promote blast fungus pathogenicity.

Blast is a devastating disease of cultivated rice, wheat, and other grasses, caused by Magnaporthe oryzae, a fungus that uses a specialized infection cell called an appressorium to breach through the host leaf cuticle. Proper morphogenesis and functionality of the M. oryzae appressorium requires the production of reactive oxygen species (ROS) by two NADPH oxidase enzymes, Nox1 and Nox2, and their regulation by NoxR. The role of a third Nox ortholog, Nox3, remains elusive. Nox2-derived ROS are essential for properly remodeling a higher-order septin ring-like structure in the base of the appressorium, a morphogenetic step critical for appressorium functionality. The precise mechanism by which Nox2-derived ROS influence the remodeling of higher-order septin structures and how the Nox2 complex is regulated in time and space remains understudied. Here, we provide a time-resolved and quantitative insight into the impact of Nox complex deletion mutants on septin and actin dynamics. Genetic and pharmacological data supports the proposed role of Nox2-derived ROS in the actin-mediated remodeling of septin structures. We describe our efforts to identify novel components of the Nox complex using proximity labeling and to understand their role in the spatial and temporal regulation of Nox2-derived ROS production. Lastly, we provide new insight into the role of Nox3 in M. oryzae