Transcription factor PpMYB73 inhibits PpPPO1 transcription and flesh browning in hydrogen sulfide-mitigated chilling injury of peach fruit

Abstract

Flesh browning, a major chilling injury (CI) symptom in peach fruit, was alleviated by hydrogen sulfide (H₂S) treatment, although its molecular mechanism remained unclear. Here, we identified five peach polyphenol oxidase genes (PpPPO), with PpPPO1 exhibiting the highest expression but inhibited by H₂S application during CI development. Chlorogenic acid (CGA), the dominant phenolic in peach fruit, was reduced in fruit transiently overexpressing PpPPO1. Molecular docking confirmed that PpPPO1 binds CGA via hydrogen bonds and hydrophobic interactions. PpPPO1 may act as the main contributor to enzymatic browning in peach fruit. H₂S treatment upregulated PpMYB73 expression, an R2R3-MYB transcription repressor, and enhanced its suppression of PpPPO1 transcription, thereby negatively regulating phenolic oxidation. Transient overexpression of PpMYB73 caused a reduction in PpPPO1 expression and PPO activity, increasing CGA accumulation and thereby suppressing soluble quinones production and flesh browning in peach fruit. While transiently silencing PpMYB73 increased soluble quinones content and exacerbated flesh browning, further confirming the inhibitory role of PpMYB73 in flesh browning. Collectively, our findings established that PpMYB73 acted as a transcriptional repressor of PpPPO1 expression, implicating H₂S-alleviated CI in peach fruit, and uncovered a novel regulatory network controlling CI.