Husk scald in pomegranates is a programmed stress-induced senescence event triggered by water loss and exacerbated by low RH

Husk scald (HS) is a major browning disorder in pomegranates that compromises marketability and postharvest quality. This study investigated the physiological and biochemical mechanisms driving HS under contrasting relative humidity (RH) levels. Pomegranates (cv. Wonderful) were stored at 55% and 95% RH for 70 days at 11°C. Low RH accelerated water loss, triggering a signaling cascade initiated by jasmonic acid (JA) accumulation. JA activated NOX-mediated ROS generation, which induced abscisic acid (ABA) and established feedback amplification of both hormones. These hormonal shifts increased reactive oxygen species (ROS) production, driven by higher NADPH oxidase (NOX) activity, leading to greater electrolyte leakage (EL) and malondialdehyde (MDA) levels. Significant enzymatic reprogramming was observed, with increased activity of phenylalanine ammonia-lyase (PAL), polyphenol oxidase (PPO), and catalase (CAT). Phenolic substrates, including trans-cinnamic and coumaric acids, accumulated under low RH, fueling PPO-driven oxidation and browning. Superoxide dismutase (SOD) activity remained stable, indicating insufficient ROS scavenging capacity to offset the stress. Conversely, high RH minimized water loss and stabilized hormonal and phenolic levels, significantly delaying HS. Our results provide mechanistic evidence that HS is a programmed, stress-induced senescence event rather than a stochastic physiological disorder. These findings emphasize that mitigating HS requires targeted strategies—such as precision RH management, CA/MAP, or signaling inhibitors—that address the underlying hormonal triggers of the senescence cascade.