Sun Shihang, Fang Jinbao, Lin Miaomiao, Hu Chungen, Qi Xiujuan, Chen Jinyong, Zhong Yunpeng, Muhammad Abid, Li Zhi, Li Yukuo
Key Laboratory for Fruit Tree Growth, Development and Quality Control, Zhengzhou Fruit Research Institute, Chinese Academy of Agricultural Sciences, Zhengzhou, China.
Key Laboratory of Horticultural Plant Biology (Ministry of Education), College of Horticulture and Forestry Science, Huazhong Agricultural University, Wuhan, China.
Front Plant Sci. 2021 Jun 1;12:628969. doi: 10.3389/fpls.2021.628969. eCollection 2021.
Cold stress poses a serious treat to cultivated kiwifruit since this plant generally has a weak ability to tolerate freezing tolerance temperatures. Surprisingly, however, the underlying mechanism of kiwifruit's freezing tolerance remains largely unexplored and unknown, especially regarding the key pathways involved in conferring this key tolerance trait. Here, we studied the metabolome and transcriptome profiles of the freezing-tolerant genotype KL () and freezing-sensitive genotype RB (), to identify the main pathways and important metabolites related to their freezing tolerance. A total of 565 metabolites were detected by a wide-targeting metabolomics method. Under (-25°C) cold stress, KEGG (Kyoto Encyclopedia of Genes and Genomes) pathway annotations showed that the flavonoid metabolic pathways were specifically upregulated in KL, which increased its ability to scavenge for reactive oxygen species (ROS). The transcriptome changes identified in KL were accompanied by the specific upregulation of a codeinone reductase gene, a chalcone isomerase gene, and an anthocyanin 5-aromatic acyltransferase gene. Nucleotides metabolism and phenolic acids metabolism pathways were specifically upregulated in RB, which indicated that RB had a higher energy metabolism and weaker dormancy ability. Since the LPCs (LysoPC), LPEs (LysoPE) and free fatty acids were accumulated simultaneously in both genotypes, these could serve as biomarkers of cold-induced frost damages. These key metabolism components evidently participated in the regulation of freezing tolerance of both kiwifruit genotypes. In conclusion, the results of this study demonstrated the inherent differences in the composition and activity of metabolites between KL and RB under cold stress conditions.
低温胁迫对栽培猕猴桃构成严重威胁，因为这种植物通常耐受冻害温度的能力较弱。然而，令人惊讶的是，猕猴桃耐寒性的潜在机制在很大程度上仍未被探索和了解，尤其是关于赋予这种关键耐受特性的关键途径。在此，我们研究了耐寒基因型KL（）和冻敏基因型RB（）的代谢组和转录组图谱，以确定与其耐寒性相关的主要途径和重要代谢物。通过广泛靶向代谢组学方法共检测到565种代谢物。在（-25°C）低温胁迫下，京都基因与基因组百科全书（KEGG）途径注释显示黄酮类代谢途径在KL中特异性上调，这增强了其清除活性氧（ROS）的能力。在KL中鉴定出的转录组变化伴随着可待因酮还原酶基因、查尔酮异构酶基因和花青素5-芳香酰基转移酶基因的特异性上调。核苷酸代谢和酚酸代谢途径在RB中特异性上调，这表明RB具有较高的能量代谢和较弱的休眠能力。由于溶血磷脂酰胆碱（LPCs）、溶血磷脂酰乙醇胺（LPEs）和游离脂肪酸在两种基因型中同时积累，这些可作为冷诱导霜冻损害的生物标志物。这些关键代谢成分显然参与了两种猕猴桃基因型耐寒性的调节。总之，本研究结果表明了低温胁迫条件下KL和RB之间代谢物组成和活性的内在差异。
