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一种新型的 MYB 转录因子调控抗坏血酸的合成并影响其对冷胁迫的耐受性。

A novel MYB transcription factor regulates ascorbic acid synthesis and affects cold tolerance.

机构信息

College of Horticulture, State Key Laboratory of Crop Genetics and Germplasm Enhancement, Nanjing Agricultural University, Nanjing, China.

出版信息

Plant Cell Environ. 2019 Mar;42(3):832-845. doi: 10.1111/pce.13387. Epub 2018 Aug 16.

Abstract

Dehydroascorbate reductase (DHAR) plays an important role in stress responses, but the transcriptional regulation of DHAR in response to abiotic stress is still poorly understood. In this study, we isolated a novel R2R3-type MYB transcription factor from Pyrus betulaefolia by yeast one-hybrid screening, designated as PbrMYB5. PbrMYB5 was localized in the nucleus and could bind specifically to the promoter of PbrDHAR2. PbrMYB5 was greatly induced by cold and salt but slightly by dehydration. Overexpression of PbrMYB5 in tobacco conferred enhanced tolerance to chilling stresses, whereas down-regulation of PbrMYB5 in P. betulaefolia by virus-induced gene silencing resulted in elevated chilling sensitivity. Transgenic tobacco exhibited higher expression levels of NtDHAR2 and accumulated larger amount of ascorbic acid (AsA) than the wild-type plants. Virus-induced gene silencing of PbrMYB5 in P. betulaefolia down-regulated PbrDHAR2 abundance and decreased AsA level, accompanied by an increased sensitivity to the chilling stress. Taken together, these results demonstrated that PbrMYB5 was an activator of AsA biosynthesis and may play a positive role in chilling tolerance, at least in part, due to the modulation of AsA synthesis by regulating the PbrDHAR2 expression.

摘要

脱氢抗坏血酸还原酶(DHAR)在应激反应中发挥重要作用,但 DHAR 对非生物胁迫的转录调控仍知之甚少。本研究通过酵母单杂交筛选从梨中分离出一种新型 R2R3 型 MYB 转录因子,命名为 PbrMYB5。PbrMYB5 定位于细胞核内,可特异性结合 PbrDHAR2 启动子。PbrMYB5 受冷胁迫和盐胁迫强烈诱导,但受干旱胁迫诱导轻微。过量表达 PbrMYB5 可增强烟草对冷胁迫的耐受性,而梨中 PbrMYB5 的病毒诱导基因沉默导致冷胁迫敏感性增加。转基因烟草的 NtDHAR2 表达水平高于野生型,积累的抗坏血酸(AsA)量也多于野生型。梨中 PbrMYB5 的病毒诱导基因沉默下调了 PbrDHAR2 的丰度,降低了 AsA 水平,同时对冷胁迫的敏感性增加。综上所述,这些结果表明 PbrMYB5 是 AsA 生物合成的激活剂,可能通过调节 PbrDHAR2 的表达来积极参与冷胁迫耐受,至少部分原因是通过调节 AsA 合成。

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