| Summary: | Breeding crops with enhanced immunity is an effective strategy to reduce yield loss caused by pathogens. The <i>constitutive expresser of pathogenesis-related genes</i> (<i>cpr5</i>) mutant shows enhanced pathogen resistance but retarded growth; thus, it restricts the application of <i>cpr5</i> in breeding crops with disease resistance. Reactive oxygen species (ROS) play important roles in plant growth and defense. In this study, we determined that the <i>cpr5</i> mutant exhibited excessive ROS accumulation. However, the mutation of respiratory burst oxidase homolog D (RBOHD), a reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase responsible for the production of ROS signaling in plant immunity, did not suppress excessive ROS levels in <i>cpr5</i>. Furthermore, the <i>cpr5</i> mutant showed low levels of ascorbate peroxidase 1 (APX1), an important cytosolic ROS-scavenging enzyme. <i>APX1</i> overexpression in the <i>cpr5</i> background removed excessive ROS and restored the pleiotropic growth phenotype. Notably, <i>APX1</i> overexpression did not reduce the resistance of <i>cpr5</i> mutant to virulent strain <i>Pseudomonas syringae</i> pv. <i>tomato</i> (<i>Pst</i>) DC3000 and avirulent strain <i>Pst</i> DC3000 (<i>avrRpt2</i>). These results suggest that the removal of excessive ROS by <i>APX1</i> overexpression restored the <i>cpr5</i> growth phenotype while conserving pathogen resistance. Hence, our study provides a theoretical and empirical basis for utilizing CPR5 in the breeding of crops with disease resistance by effective oxidative stress management via APX1 expression.
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