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Cr3a, a candidate gene conferring fruit cracking resistance, was fine-mapped in an introgression line of Solanum lycopersicum L.

In the cultivation and production of tomato (Solanum lycopersicum L.), fruit cracking is a prevalent and detrimental issue that significantly impacts the esthetic quality and commercial value of the fruit. The complexity of the trait has resulted in a slow advancement in research aimed at identifying genes that influence tomato fruit cracking and the underlying regulatory mechanisms. In this study, a sub-introgression population for tomato crack-resistant fruit has been constructed from the cross between S. lycopersicum 1052 and Solanum pennellii LA0716, followed by 11 generations of selfing. Utilizing specifically designed InDel markers, the tomato crack-resistant gene, Cr3a, was fine-mapped, cloned, and its functionality was confirmed through transgenic and gene-knockout approaches. The precise localization of Cr3a was delineated to a 30 kb genomic region on chromosome 3, corresponding to the gene Sopen03g034650 in S. pennellii and Solyc03g115660.3 in the Heinz1706 variety. An integrated transcriptomic and metabolomic analysis of fruits with and without the Cr3a gene was finally conducted to elucidate the intricate regulatory mechanisms associated with Cr3a. The findings revealed a molecular regulatory network for tomato fruit crack resistance, characterized by 7 key metabolites, 13 pivotal genes, and 4 critical pathways: the phenylpropanoid biosynthesis pathway, the phenylalanine, tyrosine, and tryptophan biosynthesis pathway, the linolenic acid metabolism pathway, and the cysteine and methionine metabolism pathway. In summary, this research provides novel insights into the molecular underpinnings of tomato fruit crack resistance and holds substantial promise for accelerating the molecular breeding of tomatoes with enhanced fruit crack resistance.

Solanum lycopersicum

Natural variants of CsSHN1 orchestrate a temporal regulatory cascade driving fruit skin netting in cucumber.

Fruit skin netting (russeting, Rs) forms when epidermal microcracks are sealed by a suberized periderm, reducing marketability. We previously identified the Rs locus (CsSHN1), which encodes an AP2/ERF transcription factor, as a major determinant of cucumber skin netting, but how fruit growth is temporally coupled to periderm formation remains unclear. Here, we integrated population genomics, time-series multiomics, DNA affinity purification sequencing (DAP-seq), and transgenic assays to decode the CsSHN1-mediated regulatory network. Six functionally relevant CsSHN1 variants were identified across 325 cucumber accessions. Allele distribution and selective sweep analyses revealed breeding-driven selection for smooth fruit skin. Overexpression of a netted allele in a smooth background induced epidermal fissures, altered cell geometry, and increased fruit size, demonstrating a dosage-sensitive effect. Time-series transcriptomics and metabolomics of near-isogenic lines (NILs) defined 3 developmental phases of netting: early suppression of lignin and trehalose genes preceding cracks, growth-driven fissuring accompanied by cell-wall remodeling and defense activation, and maturation-stage cell-wall degradation with strong induction of ligno-suberin biosynthesis. Across the cucumber genome, DAP-seq identified approximately 8,000 in vitro CsSHN1 binding sites. These binding sites were significantly enriched for the GCC-box motif and included genes involved in cutin and suberin biosynthesis. Together, these results show that CsSHN1 orchestrates fruit skin netting through a growth-coupled temporal regulatory cascade, providing a mechanistic framework for manipulating fruit epidermal properties.

Cucumis sativus