Cytological, Phytohormone, and Transcriptomic Analyses Reveal the Key Genes and Pathways Involved in Melon Fruit Cracking

Melon fruit cracking reduces yield, increases transportation costs, and shortens shelf life, which makes the development of cracking-resistant varieties crucial for the industry’s advancement. This study investigated the pathways and genes related to melon fruit cracking through cell morphology observation, endogenous hormone analyses, and transcriptome analysis of two contrasting advanced inbred lines, the extremely crack-resistant line R2 and the crack-susceptible line R6. R2 has small, tightly packed epidermal cells with a thick cuticle, while R6 has larger, more loosely arranged epidermal cells and a significantly thinner cuticle. Hormonal analysis revealed significant differences in abscisic acid, cytokinin, gibberellin, auxin, and salicylic acid contents between R2 and R6 at various fruit developmental stages. The abscisic acid and salicylic acid content in R2 were 1.9–5.2 times and 1.5–3.6 times higher than those in R6, respectively, whereas the gibberellin content in R6 was 1.5–2.3 times higher than that in R2. Pericarp transcriptome analysis identified 4281, 6242, and 6879 differentially expressed genes (DEGs) at 20, 30, and 40 days after anthesis, respectively. Among these, 47 DEGs related to phenylpropanoid biosynthesis (ko00940) and 79 DEGs involved in plant hormone signal transduction (ko04075) were differentially expressed at two or more stages. WGCNA analysis identified six core hub genes that potentially play a role in regulating melon fruit cracking. These findings lay a foundation for further studies on the functional roles of crack-resistant genes and the breeding of crack-tolerant varieties.