A multi-omics approach reveals the effects of wax, cell wall polysaccharides and hormones on pepper skin cracking

Fruit cracking is a severe physiological disorder, affecting fruit yield and quality, and causing significant economic losses. To elucidate the molecular mechanisms underlying pepper skin cracking, we performed histological, physicochemical, metabolomics, and transcriptome analyses on A179 (cracking-susceptible) and A115 (cracking-resistant) pepper varieties. Our results showed that the cuticle was thin and split, and the cell layer with larger cell volume was deformed and raised in the cracking region of A179. The A179 fruit epidermis exhibited less deposition of most wax components, such as fatty acids, alkanes, and esters. Furthermore, the high expression of cell wall metabolism- and modification-related genes and the high pectinase and peroxidase activities in A179 fruit promoted the decomposition and decrosslinking of polysaccharide components such as protopectin, soluble pectin, and cellulose. This phenomenon contributed to aquaporin-mediated water transfer into the cell, expanding the softened cell wall, and ultimately leading to A179 skin cracking. Moreover, the contents of auxin, cytokinin and their derivatives in the peel of A179 were significantly lower than those of A115 during fruit development. The hormone/wax-gene interaction network further revealed that auxin, cytokinin, and ethylene might regulate the biosynthesis of wax components and the modification of cell wall polysaccharides through ARF2 , GH3 , and ERF1 transcription factors, thereby affecting pepper skin cracking. Collectively, our study demonstrated that cuticle thickness, cell wall polysaccharide composition, and hormone levels are key factors determining the susceptibility of pepper skin cracking.