PpPrimPol helps delay postharvest-decay in peach fruit by maintaining mitochondrial function

Peach fruit decay after postharvest, resulting in mitochondrial DNA (mtDNA) damage and mitochondrial dysfunction. PrimPol could recognize and skip DNA damage during DNA copy, and then continue the downstream replication of DNA damage, ensuring genome integrity. To explore whether PrimPol plays a role in regulating the physiology of fruit after postharvest, a mitochondrial-located PpPrimPol was cloned and over-expressed in postharvest peach fruit and tomato. The oxidative damage of peach fruit, mitochondrial reactive oxygen species (ROS) content, mitochondrial function, antioxidation-related enzymes, and relative gene expression levels in peach and tomato fruit were measured. The results displayed that the over-expression of PpPrimPol stabilized mtDNA copy number, maintained mitochondrial morphology and function, increased the scavenging rate of ROS free radicals. Meanwhile, the over-expression of PpPrimPol enhanced the activities of antioxidant enzymes and increased the expression level of antioxidant enzymes in fruit, thus maintained the quality of fruit after harvest.