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猕猴桃 bZIP 转录因子 AcePosF21 在冷胁迫下诱导抗坏血酸生物合成。

Kiwifruit bZIP transcription factor AcePosF21 elicits ascorbic acid biosynthesis during cold stress.

机构信息

Wuhan Botanical Garden, Chinese Academy of Sciences, Jiufeng 1 Road, Wuhan 430074, Hubei, China.

College of Life Sciences, University of Chinese Academy of Sciences, 19A Yuquan Road, Beijing 100049, China.

出版信息

Plant Physiol. 2023 May 31;192(2):982-999. doi: 10.1093/plphys/kiad121.

Abstract

Cold stress seriously affects plant development, resulting in heavy agricultural losses. L-ascorbic acid (AsA, vitamin C) is an antioxidant implicated in abiotic stress tolerance and metabolism of reactive oxygen species (ROS). Understanding whether and how cold stress elicits AsA biosynthesis to reduce oxidative damage is important for developing cold-resistant plants. Here, we show that the accumulation of AsA in response to cold stress is a common mechanism conserved across the plant kingdom, from single-cell algae to angiosperms. We identified a basic leucine zipper domain (bZIP) transcription factor (TF) of kiwifruit (Actinidia eriantha Benth.), AcePosF21, which was triggered by cold and is involved in the regulation of kiwifruit AsA biosynthesis and defense responses against cold stress. AcePosF21 interacted with the R2R3-MYB TF AceMYB102 and directly bound to the promoter of the gene encoding GDP-L-galactose phosphorylase 3 (AceGGP3), a key conduit for regulating AsA biosynthesis, to up-regulate AceGGP3 expression and produce more AsA, which neutralized the excess ROS induced by cold stress. On the contrary, VIGS or CRISPR-Cas9-mediated editing of AcePosF21 decreased AsA content and increased the generation of ROS in kiwifruit under cold stress. Taken together, we illustrated a model for the regulatory mechanism of AcePosF21-mediated regulation of AceGGP3 expression and AsA biosynthesis to reduce oxidative damage by cold stress, which provides valuable clues for manipulating the cold resistance of kiwifruit.

摘要

冷胁迫严重影响植物的生长发育,导致农业减产严重。抗坏血酸(AsA,维生素 C)是一种与非生物胁迫耐受和活性氧(ROS)代谢有关的抗氧化剂。了解冷胁迫是否以及如何引发 AsA 生物合成以减少氧化损伤,对于培育抗寒植物非常重要。在这里,我们表明,植物界从单细胞藻类到被子植物,对冷胁迫的 AsA 积累是一种保守的机制。我们鉴定了猕猴桃(Actinidia eriantha Benth.)AcePosF21 的碱性亮氨酸拉链结构域(bZIP)转录因子(TF),该因子被冷胁迫触发,参与调控猕猴桃 AsA 生物合成和防御冷胁迫的反应。AcePosF21 与 R2R3-MYB TF AceMYB102 相互作用,并直接结合编码 GDP-L-半乳糖磷酸化酶 3(AceGGP3)的基因启动子,AceGGP3 是调节 AsA 生物合成的关键途径,上调 AceGGP3 的表达并产生更多的 AsA,从而中和冷胁迫诱导的过量 ROS。相反,在冷胁迫下,VIGS 或 CRISPR-Cas9 介导的 AcePosF21 编辑降低了猕猴桃中的 AsA 含量并增加了 ROS 的产生。综上所述,我们阐明了 AcePosF21 介导的 AceGGP3 表达和 AsA 生物合成调控机制的模型,以减轻冷胁迫引起的氧化损伤,为操纵猕猴桃的抗寒性提供了有价值的线索。

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