State Key Laboratory of Crop Stress Biology for Arid Areas, College of Horticulture, Northwest A&F University, Yangling, Shaanxi, 712100, China.
Shaanxi Research Center of Apple Engineering and Technology, Yangling, Shaanxi, 712100, China.
New Phytol. 2024 Dec;244(6):2458-2473. doi: 10.1111/nph.20158. Epub 2024 Oct 3.
The sweetness of apple fruit is a key factor in the improvement of apple varieties, with fructose being the sweetest of the soluble sugars, playing a crucial role in determining the overall sweetness of the apple. Therefore, uncovering the key genes controlling fructose accumulation and deciphering the regulatory mechanisms of fructose are vitally important for the improvement of apple varieties. In this study, through BSA-seq and transcriptome analysis of the 'Changfu 2' × 'Golden Delicious' F1 hybrid population, MdNAC5 was identified as a key regulatory gene for fructose content. MdNAC5 was shown to significantly influence fructose accumulation in both apples and tomatoes. Furthermore, we conducted a detailed identification of sugar transporters and metabolic enzymes in apples, discovering that MdNAC5 can enhance fructose accumulation in vacuoles and the conversion of sucrose to fructose by binding to and activating the promoters of the vacuolar sugar transporter MdTST2 and the neutral invertase MdNINV6. Additionally, MdNAC5 regulated the MdEIN3.4-MdSWEET15a module, strengthening the unloading of sucrose in the phloem of the fruit. Our results reveal a new mechanism by which MdNAC5 regulates fructose accumulation in apples and provide theoretical foundations for improving apple sweetness through genetic modification.
苹果果实的甜度是苹果品种改良的关键因素,其中果糖是可溶性糖中最甜的一种,对苹果整体甜度的形成起着至关重要的作用。因此,揭示控制果糖积累的关键基因,解析果糖积累的调控机制,对于苹果品种的改良具有重要意义。本研究通过‘昌富 2 号’ב金冠’F1 杂种群体的 BSA-seq 和转录组分析,鉴定 MdNAC5 为影响果糖含量的关键调控基因。MdNAC5 显著影响苹果和番茄中的果糖积累。此外,我们对苹果中的糖转运蛋白和代谢酶进行了详细鉴定,发现 MdNAC5 通过与液泡糖转运蛋白 MdTST2 和中性转化酶 MdNINV6 的启动子结合并激活,促进了液泡中果糖的积累和蔗糖向果糖的转化。此外,MdNAC5 还调控 MdEIN3.4-MdSWEET15a 模块,增强了果实韧皮部中蔗糖的卸载。本研究揭示了 MdNAC5 调控苹果果糖积累的新机制,为通过遗传改良提高苹果甜度提供了理论基础。