The tomato 2-oxoglutarate-dependent dioxygenase gene SlF3HL is critical for chilling stress tolerance

The tomato 2-oxoglutarate-dependent dioxygenase gene SlF3HL is critical for chilling stress tolerance
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番茄 2-酮戊二酸依赖性双加氧酶基因 SlF3HL 对于耐冷胁迫至关重要

DOI:
10.1038/s41438-019-0127-5
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发表时间:
2019-04-06
影响因子:
8.7
通讯作者:
Zhan, Xiangqiang
Zhan, Xiangqiang
中科院分区:
农林科学1区
文献类型:
--
作者:
Hu, Tixu;Wang, Yuqin;Zhan, Xiangqiang

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低温是严重影响植物发育、生长、分布和生产力的主要逆境。在这里,我们检查了 2-酮戊二酸依赖性双加氧酶编码基因 SlF3HL 在番茄(Solanum lycopersicum cv. Alisa Craig [AC])冷应激反应中的功能。番茄中 SlF3HL 的敲低 (KD)(通过 RNA 干扰)导致对冷应激的敏感性增加,电解质渗漏、丙二醛 (MDA) 和活性氧 (ROS) 水平升高表明这一点。此外,KD 植物的脯氨酸水平降低,过氧化物酶体和超氧化物歧化酶的活性降低。 KD 植物中四个冷响应基因的表达显着降低。此外,在茉莉酸甲酯(MeJA)正常生长条件或冷胁迫条件下,AC或SlF3HL过表达植物中的幼苗生长显着高于KD植物。 SlF3HL 似乎在寒冷胁迫下正向调节 JA 积累以及 JA 生物合成和信号基因的表达。总之,这些结果表明 SlF3HL 是冷胁迫耐受性的正调节因子,并在冷胁迫耐受途径中发挥作用,可能是通过调节 JA 生物合成、JA 信号传导和 ROS 水平。
Low temperature is a major stress that severely affects plant development, growth, distribution, and productivity. Here, we examined the function of a 2-oxoglutarate-dependent dioxygenase-encoding gene, SlF3HL, in chilling stress responses in tomato (Solanum lycopersicum cv. Alisa Craig [AC]). Knockdown (KD) of SlF3HL (through RNA interference) in tomato led to increased sensitivity to chilling stress as indicated by elevated levels of electrolyte leakage, malondialdehyde (MDA) and reactive oxygen species (ROS). In addition, the KD plants had decreased levels of proline and decreased activities of peroxisome and superoxide dismutase. The expression of four cold-responsive genes was substantially reduced in the KD plants. Furthermore, seedling growth was significantly greater in AC or SlF3HL-overexpression plants than in the KD plants under either normal growth conditions with methyl jasmonate (MeJA) or chilling stress conditions. SlF3HL appears to positively regulate JA accumulation and the expression of JA biosynthetic and signaling genes under chilling stress. Together, these results suggest that SlF3HL is a positive regulator of chilling stress tolerance and functions in the chilling stress tolerance pathways, possibly by regulating JA biosynthesis, JA signaling, and ROS levels.