Xiang Hengzuo, Meng Sida, Ye Yunzhu, Han Leilei, He Yi, Cui Yiqing, Tan Changhua, Ma Jian, Qi Mingfang, Li Tianlai
College of Horticulture, Shenyang Agricultural University, Shenyang, China.
National & Local Joint Engineering Research Center of Northern Horticultural Facilities Design & Application Technology (Liaoning), Shenyang, China.
Front Plant Sci. 2023 Aug 23;14:1249760. doi: 10.3389/fpls.2023.1249760. eCollection 2023.
Malformed tomato fruit with multiple locules is a common physiological disorder that significantly affects the quality of tomatoes. Research has shown that the occurrence of malformed fruit in tomatoes is closely linked to the number of locules, and two key QTLs, and , are involved in controlling this trait. It has been observed that has a relatively weaker effect on increasing locule number, which is associated with two SNPs in the CArG repressor element downstream of the . However, the precise molecular mechanism underlying is not yet fully understood. In this study, we investigated the role of in tomato locule development. We found that the number of floral organs and fruit locules significantly increased in tomato knockout mutants. Additionally, these mutants showed higher expression levels of the during carpel formation. Through cDNA library construction and yeast one-hybrid screening, we identified the MADS-box transcription factor SlSEP3, which was found to bind to . Furthermore, we observed an increase in floral organs and fruit locules similar to the plant on silencing plants. However, it should be noted that the site is located after the 3' untranslated region (UTR) of in the tomato genome. As a result, SlSEP3 may not be able to exert regulatory functions on the promoter of the gene like other transcription factors. In the yeast two-hybrid assay, we found that several histone deacetylases (SlHDA1, SlHDA3, SlHDA4, SlHDA5, SlHDA6, SlHDA7, and SlHDA8) can interact with SlSEP3. This indicated that SlSEP3 can recruit these proteins to repress nucleosome relaxation, thereby inhibiting transcription and affecting the number of locules in tomato fruit. Therefore, our findings reveal a new mechanism for playing a significant role in the genetic pathway regulating tomato locule development.
具有多个心室的畸形番茄果实是一种常见的生理病害，严重影响番茄品质。研究表明，番茄畸形果实的发生与心室数量密切相关，两个关键的数量性状位点（QTL）参与控制这一性状。据观察，[未提及的某个因素]对增加心室数量的作用相对较弱，这与[未提及的某个基因]下游CArG阻遏元件中的两个单核苷酸多态性（SNP）有关。然而，[未提及的某个因素]背后的确切分子机制尚未完全明确。在本研究中，我们探究了[未提及的某个因素]在番茄心室发育中的作用。我们发现，番茄[未提及的某个基因]敲除突变体中花器官和果实心室的数量显著增加。此外，这些突变体在心皮形成过程中[未提及的某个基因]的表达水平较高。通过构建cDNA文库和酵母单杂交筛选，我们鉴定出MADS盒转录因子SlSEP3，发现它能与[未提及的某个基因]结合。此外，我们观察到在[未提及的某个基因]沉默植株上，花器官和果实心室数量增加，类似于[未提及的某个基因]敲除植株。然而，需要注意的是，[未提及的某个基因]位点位于番茄基因组中[未提及的某个基因]的3'非翻译区（UTR）之后。因此，SlSEP3可能无法像其他转录因子那样对该基因的启动子发挥调控功能。在酵母双杂交试验中，我们发现几种组蛋白脱乙酰酶（SlHDA1、SlHDA3、SlHDA4、SlHDA5、SlHDA6、SlHDA7和SlHDA8）能与SlSEP3相互作用。这表明SlSEP3可以招募这些蛋白质来抑制核小体松弛，从而抑制[未提及的某个基因]转录并影响番茄果实心室数量。因此，我们的研究结果揭示了[未提及的某个因素]在调控番茄心室发育的遗传途径中发挥重要作用的新机制。
