Abstract:

Fruit firmness is a key indicator of fruit maturity and directly influences fruit quality, shelf life, and storage potential, thereby determining its commercial value. The formation, maintenance, and softening of fruit firmness are complex biological processes involving a series of physiological and molecular changes. Alterations in cell wall components — such as pectin, cellulose, hemicellulose, and lignin — mediated by cell wall-modifying enzymes, including pectinases, β-galactosidases, xyloglucan endotransglucanases/hydrolases, and expansins directly affect fruit firmness. The degradation of starch, which helps maintain cell turgor, also contributes to firmness changes. Fruit softening is coordinately regulated by multiple phytohormones and transcription factors. In climacteric fruits, ethylene regulates softening through the ACS-ACO synthesis pathway and the ETR-EIN3/ERFs signaling network, while abscisic acid activates the softening in non-climacteric fruits via the NCED-PYR/PYL/RCAE-PP2C-SnRK2 cascade. Other phytohormones such as auxin, gibberellin, and brassinosteroid interact directly or indirectly with ethylene and ABA signaling pathways to collectively regulate fruit softening. Transcription factors, including MADS-box, MYB, NAC, and WRKY proteins, regulate fruit firmness by modulating genes involved in cell wall or starch metabolism. Hormone response factors such as ERF and ARF mediate hormone signal transduction to control the biosynthesis and degradation of hormones like ethylene and ABA, thereby participating in the maintenance and softening of fruit firmness. Additionally, various TFs also regulate fruit softening by mediating complex hormonal crosstalk. Recent studies have shown that post-translational modifications such as phosphorylation and ubiquitination, along with epigenetic mechanisms including DNA methylation and histone acetylation, also synergistically regulate fruit firmness. Based on high-density genetic map and genome-wide association analyses, multiple quantitative trait loci (QTL) related to fruit firmness have been identified, with cell wall metabolism-related genes, hormone biosynthesis and signaling components, and transcription factors emerging as key candidates. This review systematically summarizes the factors and genetic loci affecting fruit firmness, focusing on molecular mechanisms mediated by phytohormone biosynthesis and signal transduction, as well as TFs that regulate cell wall modification, starch degradation, hormonal signaling, and hormonal crosstalk underlying firmness regulation. Our aim is to provide a theoretical reference for in-depth analysis of the fruit firmness regulatory network and to propose potential targets for breeding cultivars with improved storage tolerance and fruit quality.

Key words: fruit firmness, cell wall metabolism, starch degradation, phytohormone, transcription regulation, post-translational modification, epigenetic regulation, quantitative trait loci (QTL)