Postharvest fruit softening is a critical determinant of fruit shelf life, significantly influencing mechanical damage susceptibility, pathogen invasion, and consumer preference. Collectively, these factors lead to substantial losses in the fruit industry. The structural modifications of cell wall and cuticle during ripening primarily govern fruit softening. The objective of this review is to synthesize recent advances and provide a comprehensive analysis of the molecular mechanisms underlying this process. In this review, we provide a comprehensive analysis of cell wall composition and softening-associated cell wall remodeling proteins. We examine recent advances in manipulating single or multiple genes encoding cell wall-modifying proteins that influence fruit softening, and identify key transcription factors regulating the expression of these gene networks. This review synthesizes current understanding of the molecular mechanisms governing fruit ripening, providing a foundation for future research in postharvest biology.

Leaf senescence is a critically regulated developmental process that determines crop yield and quality. MYB and NAC transcription factors (TFs) are central regulators within this network, yet the crosstalk between these TF families and their connection to the gibberellin (GA) pathway remain poorly understood. This study revealed that overexpression of DIV1, a MYB-like TF, leads to significantly reduced chlorophyll content and precocious leaf senescence. Based on the public transcriptome profiling of DIV1-overexpression leaves, 37 senescence-associated differentially expressed genes (DEGs), including the highly upregulated NAC59 and NAC92, were identified. Molecular assays confirmed that DIV1 directly binds to the promoters of NAC59 and NAC92 and activates their transcription. Meanwhile, yeast two-hybrid and split-luciferase assays demonstrated that DIV1 physically interacts with the GA biosynthetic enzyme ent-kaurene oxidase (KO1) both in vitro and in vivo. The promoted senescence phenotype in DIV1-overexpression lines was rescued by treatment with paclobutrazol (PAC), a GA biosynthesis inhibitor. In summary, our findings reveal a dual mechanism whereby DIV1 integrates the GA pathway and NAC-mediated transcription to regulate leaf senescence. This work provides new insights into the coordination between MYB and NAC TFs during hormone-mediated senescence.

Background: Malus sieversii, the wild ancestor of cultivated apples, possesses high stress tolerance and rich nutritional value but suffers from low fruit firmness. Jasmonate-ZIM (JAZ) domain proteins are key repressors of jasmonic acid (JA) signaling, yet their roles in fruit softening remain largely unexplored, especially in M. sieversii. Methods and results: In this study, we performed a genome-wide identification of the JAZ gene family in M. sieversii and characterized their structural features, phylogenetic relationships, chromosomal distribution, promoter cis-elements, expression patterns, and protein interactions. A total of 18 MsiJAZ genes were identified, which could be classified into six subfamilies. Most members are predicted to localize in the nucleus, while three are also potentially targeted to chloroplasts. The MsiJAZ genes are unevenly distributed across ten chromosomes and are enriched in light-, ABA-, and drought-responsive cis-elements. Expression analysis under storage and 1-MCP treatments revealed both shared and divergent responses among selected MsiJAZ genes. Notably, MsiJAZ1 was significantly repressed by storage but induced by 1-MCP and physically interacted with MsiPUB24 (PLANT U-BOX 24), an E3 ubiquitin ligase involved in ethylene-mediated softening. These results suggest that MsiJAZ1 may participate in a novel CORONATINE INSENSITIVE 1 (COI1)-independent degradation pathway and mediate ethylene–JA crosstalk during fruit softening. Conclusions: This study provides a comprehensive characterization of the JAZ family in M. sieversii and lays a foundation for further functional studies on JA signaling in apple fruit softening.