Clarifying physiological and molecular mechanisms for Husk Scald development in pomegranate fruit

The pomegranate (Punica granatum L.), which contains high levels of health-promoting compounds, has received much attention in recent decades. Fruit storage potential ranges from 3 to 4 months in air and from 4 to 6 months in Controlled Atmospheres (CA) with 3-5% oxygen and 10-15% carbon dioxide. Storage life is limited by decay, chilling injury, weight loss, and husk scald. In particular, husk scald (HS) limits pomegranate long-term storage at favorable temperatures. HS appears as skin browning which expands from stem end towards the blossom end during handling or long-term storage (10 – 12 weeks) at 6‐10 ̊C. Even though HS symptoms are limited to external appearance, it may still significantly reduce pomegranate fruit marketability. A number of postharvest treatments have been proposed to prevent husk scald, including atmospheric modifications, intermittent warming, coatings, and exposure to 1‐MCP. Long-term storage may induce phenolic compounds accumulation, affect organelles membranes, and activate browning enzymes like polyphenol oxidases (PPO) and peroxidases (POD). Due to oxidation of tannins and phenolics, scalding becomes visible. There is no complete understanding of the etiology and biochemistry of HS. This review discusses the hypothesized mechanism of HS based on recent research, its association to postharvest treatments, and their possible targets.