College of Horticulture Science and Engineering, Shandong Agricultural University, 61 Daizong Road, Tai'an, 271018, China.
State Key Laboratory of Crop Biology, Shandong Agricultural University, 61 Daizong Road, Tai'an, 271018, China.
BMC Genet. 2019 Aug 1;20(1):65. doi: 10.1186/s12863-019-0746-8.
Fruit set after successful pollination is key for the production of sweet cherries, and a low fruit-setting rate is the main problem in production of this crop. As gibberellin treatment can directly induce parthenogenesis and satisfy the hormone requirement during fruit growth and development, such treatment is an important strategy for improving the fruit-setting rate of sweet cherries. Previous studies have mainly focused on physiological aspects, such as fruit quality, fruit size, and anatomical structure, whereas the molecular mechanism remains clear.
In this study, we analyzed the transcriptome of 'Meizao' sweet cherry fruit treated with gibberellin during the anthesis and hard-core periods to identify genes associated with parthenocarpic fruit set. A total of 25,341 genes were identified at the anthesis and hard-core stages, 765 (681 upregulated, 84 downregulated) and 186 (141 upregulated, 45 downregulated) of which were significant differentially expressed genes (DEGs) at the anthesis and the hard-core stages after gibberellin 3 (GA3) treatment, respectively. Based on DEGs between the control and GA3 treatments, the GA3 response mainly involves parthenocarpic fruit set and cell division. Exogenous gibberellin stimulated sweet cherry fruit parthenocarpy and enlargement, as verified by qRT-PCR results of related genes as well as the parthenocarpic fruit set and fruit size. Based on our research and previous studies in Arabidopsis thaliana, we identified key genes associated with parthenocarpic fruit set and cell division. Interestingly, we observed patterns among sweet cherry fruit setting-related DEGs, especially those associated with hormone balance, cytoskeleton formation and cell wall modification.
Overall, the result provides a possible molecular mechanism regulating parthenocarpic fruit set that will be important for basic research and industrial development of sweet cherries.
授粉成功后的结实率是甜樱桃生产的关键，结实率低是该作物生产的主要问题。由于赤霉素处理可以直接诱导孤雌生殖，并满足果实生长发育过程中激素的需求，因此这种处理是提高甜樱桃结实率的重要策略。以前的研究主要集中在生理方面，如果实品质、果实大小和解剖结构，而分子机制尚不清楚。
本研究在盛花期末和硬核期末分析了甜樱桃果实经赤霉素处理后的转录组，以鉴定与单性结实果实结实相关的基因。在盛花期和硬核期共鉴定出 25341 个基因，其中有 765 个（681 个上调，84 个下调）和 186 个（141 个上调，45 个下调）基因在赤霉素 3（GA3）处理后的盛花期和硬核期差异表达显著（DEGs）。基于对照和 GA3 处理之间的 DEGs，GA3 反应主要涉及单性结实果实的形成和细胞分裂。外源赤霉素刺激甜樱桃果实单性结实和增大，这通过相关基因的 qRT-PCR 结果以及单性结实果实的形成和果实大小得到验证。基于我们的研究和拟南芥的先前研究，我们鉴定了与单性结实果实形成和细胞分裂相关的关键基因。有趣的是，我们观察到了甜樱桃果实结实相关 DEGs 之间的模式，特别是与激素平衡、细胞骨架形成和细胞壁修饰相关的基因。
总之，该结果为单性结实果实的形成提供了一个可能的分子机制，这对甜樱桃的基础研究和工业发展将是重要的。
