Li Xueou, Xu Dawei, Zhang Lida, Zhao Lingxia
Department of Plant Science, School of Agriculture and Biology, Shanghai Jiao Tong University, 800 Dongchuan Road, Shanghai, 200240, China.
Joint Tomato Research Institute, School of Agriculture and Biology, Shanghai Jiao Tong University, 800 Dongchuan Road, Shanghai, 200240, China.
BMC Plant Biol. 2025 May 27;25(1):704. doi: 10.1186/s12870-025-06749-7.
Delayed fruit softening in tomato (Solanum lycopersicum) is highly desirable for extending shelf life, facilitating long-distance transportation, and reducing post-harvest losses caused by mechanical damage. Fruit softening is a natural ripening process characterized by the increased expression of genes involved in cell wall modification, leading to the breakdown of cell wall polysaccharides and the gradual disintegration of cellular structure. The yft1 mutant (yellow-fruited tomato 1, originally designated n3122) exhibits inhibited ethylene production, preventing normal ripening and resulting in firmer fruit. Concurrently, yft1 shows significant downregulation of several genes associated with cell wall degradation, including endoglucanase SlCEL2 and EXPANSIN SlEXP1. Both genes exhibit similar expression patterns, peaking during ripening, suggesting their importance in fruit softening. To investigate this further, RNAi silencing lines targeting SlCEL2 and SlEXP1 were generated. The double mutant, slcel2 slexp1, displayed increased firmness at the red ripe stage (54 days post-anthesis, dpa), whereas the single mutants showed similar softening to the wild-type M82. Anatomical analysis at 54 dpa revealed enhanced cell wall structure, slightly increased cuticle thickness, and significantly higher pericarp cellulose content in slcel2 slexp1 compared to M82, slcel2, and slexp1. Furthermore, this study found that SlEXP1 expression was significantly upregulated in slcel2 fruit, compared to M82 (wild type), at 54 dpa. This suggests a compensatory transcriptional regulation between these two genes in tomato fruit, potentially aimed at maintaining normal softening during ripening. These findings demonstrate that SlCEL2 and SlEXP1 act synergistically in cellulose degradation during tomato ripening, and promoting fruit softening.
番茄（Solanum lycopersicum）果实延迟软化对于延长货架期、便于长途运输以及减少机械损伤造成的采后损失非常重要。果实软化是一个自然成熟过程，其特征是参与细胞壁修饰的基因表达增加，导致细胞壁多糖分解和细胞结构逐渐解体。yft1突变体（黄果番茄1，最初命名为n3122）表现出乙烯生成受到抑制，阻止了正常成熟，导致果实更硬。同时，yft1显示出与细胞壁降解相关的几个基因显著下调，包括内切葡聚糖酶SlCEL2和扩张蛋白SlEXP1。这两个基因表现出相似的表达模式，在成熟过程中达到峰值，表明它们在果实软化中具有重要作用。为了进一步研究这一点，构建了靶向SlCEL2和SlEXP1的RNA干扰沉默系。双突变体slcel2 slexp1在红熟期（花后54天，dpa）表现出硬度增加，而单突变体与野生型M82表现出相似的软化程度。在54 dpa时的解剖分析表明，与M82、slcel2和slexp1相比，slcel2 slexp1的细胞壁结构增强，角质层厚度略有增加，果皮纤维素含量显著更高。此外，本研究发现，在54 dpa时，与M82（野生型）相比，slcel2果实中SlEXP1的表达显著上调。这表明这两个基因在番茄果实中存在补偿性转录调控，可能旨在维持成熟过程中的正常软化。这些发现表明，SlCEL2和SlEXP1在番茄成熟过程中的纤维素降解中协同作用，促进果实软化。
