The redox homeostasis of plant cells depends upon a balance between generation of reactive oxygen species (ROS) and quenching of ROS by antioxidants, and this balance influences susceptibility to pathogens and other stresses (Trchounian et al., 2016). Plants commonly produce ROS such as superoxide (O −2 ) and hydrogen peroxide (H 2 O 2 ) in response to biotic and abiotic stresses, resulting in an oxidative response (Suzuki et al., 2012;Trchounian et al., 2016). Depending upon the timing, magnitude, and persistence of ROS accumulation, stress-responsive oxidative responses may be adaptive to the plant or may contribute to symptom development. Prolonged and uncontrolled ROS production can damage cell membranes, nucleic acids, and proteins in plant cells; this results in oxidative stress and can in some cases facilitate pathogen infection in compatible interactions (Demidchik, 2015;Petrov et al., 2015;Rossi et al., 2017). Moreover, rapid and transient ROS accumulation can function to trigger plant immune responses, and is commonly observed in the plant apoplast at the site of infection during incompatible interactions with pathogens (Apel & Hirt, 2004;Lamb & Dixon, 1997). This so-called oxidative burst in the apoplast typically relies on generation of O − 2 by NADPH oxidases at the plasma membrane and conversion of O − 2 to H 2 O 2 by superoxide dismutase; H 2 O 2 may also be generated by cell wall peroxidases (