Chen Yifan, Gao Wenzheng, Zhu Yu, Qiu Shuliang, Qiu Zhuoyao, Dong Chenchen, Liu Ziteng, Du Yongchen, Li Junming, Huang Zejun, Li Xin, Liu Lei, Liu Liwang, Wang Xiaoxuan
State Key Laboratory of Vegetable Biobreeding, Institute of Vegetables and Flowers, Chinese Academy of Agricultural Sciences, Beijing, 100081, China.
College of Horticulture, Nanjing Agricultural University, Nanjing, 210095, China.
Plant J. 2025 Apr;122(2):e70184. doi: 10.1111/tpj.70184.
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.
在番茄（Solanum lycopersicum L.）的栽培和生产中，果实开裂是一个普遍且有害的问题，严重影响果实的外观品质和商业价值。该性状的复杂性导致旨在鉴定影响番茄果实开裂的基因及其潜在调控机制的研究进展缓慢。在本研究中，通过番茄品种1052与潘那利番茄（Solanum pennellii）LA0716杂交构建了一个番茄抗裂果实的渐渗亚群体，随后进行了11代自交。利用专门设计的InDel标记，对番茄抗裂基因Cr3a进行了精细定位、克隆，并通过转基因和基因敲除方法证实了其功能。Cr3a被精确定位到3号染色体上一个30 kb的基因组区域，对应于潘那利番茄中的基因Sopen03g034650和Heinz1706品种中的Solyc03g115660.3。最后，对具有和不具有Cr3a基因的果实进行了转录组和代谢组综合分析，以阐明与Cr3a相关的复杂调控机制。研究结果揭示了一个番茄果实抗裂的分子调控网络，其特征包括7种关键代谢物、13个关键基因和4条关键途径：苯丙烷生物合成途径、苯丙氨酸、酪氨酸和色氨酸生物合成途径、亚麻酸代谢途径以及半胱氨酸和甲硫氨酸代谢途径。总之，本研究为番茄果实抗裂的分子基础提供了新的见解，并有望加速培育具有更强果实抗裂性的番茄分子育种进程。
