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转录因子 AtGLK1 通过作用于 MYBL2 的上游来遗传调控拟南芥中蔗糖诱导的花青素生物合成。

The transcription factor AtGLK1 acts upstream of MYBL2 to genetically regulate sucrose-induced anthocyanin biosynthesis in Arabidopsis.

机构信息

College of Agronomy/Key Laboratory of Crop Physiology, Ecology and Genetic Breeding, Ministry of Education, Jiangxi Agricultural University, Nanchang, 330045, China.

出版信息

BMC Plant Biol. 2021 May 28;21(1):242. doi: 10.1186/s12870-021-03033-2.

DOI:10.1186/s12870-021-03033-2
PMID:34049482
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8162001/
Abstract

BACKGROUND

The regulation of anthocyanin biosynthesis by various factors including sugars, light and abiotic stresses is mediated by numerous regulatory factors acting at the transcriptional level. Here experimental evidence was provided in order to demonstrate that the nuclear GARP transcription factor AtGLK1 plays an important role in regulating sucrose-induced anthocyanin biosynthesis in Arabidopsis.

RESULTS

The results obtained using real-time quantitative PCR and GUS staining assays revealed that AtGLK1 was mainly expressed in the green tissues of Arabidopsis seedlings and could be induced by sucrose. The loss-of-function glk1 glk2 double mutant has lower anthocyanin levels than the glk2 single mutant, although it has been determined that loss of AtGLK1 alone does not affect anthocyanin accumulation. Overexpression of AtGLK1 enhances the accumulation of anthocyanin in transgenic Arabidopsis seedlings accompanied by increased expression of anthocyanin biosynthetic and regulatory genes. Moreover, we found that AtGLK1 also participates in plastid-signaling mediated anthocyanin accumulations. Genetic, physiological, and molecular biological approaches demonstrated that AtGLK1 acts upstream of MYBL2, which is a key negative regulator of anthocyanin biosynthesis, to genetically regulate sucrose-induced anthocyanin biosynthesis.

CONCLUSION

Our results indicated that AtGLK1 positively regulates sucrose-induced anthocyanin biosynthesis in Arabidopsis via MYBL2.

摘要

背景

各种因素（包括糖、光和非生物胁迫）对花色苷生物合成的调控是通过许多在转录水平起作用的调控因子介导的。本文提供了实验证据，证明核 GARP 转录因子 AtGLK1 在调节拟南芥中蔗糖诱导的花色苷生物合成中起重要作用。

结果

实时定量 PCR 和 GUS 染色分析的结果表明，AtGLK1 在拟南芥幼苗的绿色组织中主要表达，并能被蔗糖诱导。glk1 glk2 双突变体的功能丧失比 glk2 单突变体的花色苷水平更低，尽管已经确定单独缺失 AtGLK1 并不影响花色苷的积累。AtGLK1 的过表达增强了转基因拟南芥幼苗中花色苷的积累，同时伴随着花色苷生物合成和调控基因的表达增加。此外，我们发现 AtGLK1 还参与了质体信号介导的花色苷积累。遗传、生理和分子生物学方法表明，AtGLK1 通过 MYBL2 作为花色苷生物合成的关键负调控因子，在上游调控蔗糖诱导的花色苷生物合成。

结论

我们的结果表明，AtGLK1 通过 MYBL2 正向调控拟南芥中蔗糖诱导的花色苷生物合成。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac2c/8162001/c4d75546c042/12870_2021_3033_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac2c/8162001/86a3c427aa4c/12870_2021_3033_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac2c/8162001/1de25c69cd15/12870_2021_3033_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac2c/8162001/d71f015542de/12870_2021_3033_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac2c/8162001/1af62a7c03ca/12870_2021_3033_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac2c/8162001/18fa87307061/12870_2021_3033_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac2c/8162001/c4d75546c042/12870_2021_3033_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac2c/8162001/86a3c427aa4c/12870_2021_3033_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac2c/8162001/1de25c69cd15/12870_2021_3033_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac2c/8162001/d71f015542de/12870_2021_3033_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac2c/8162001/1af62a7c03ca/12870_2021_3033_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac2c/8162001/18fa87307061/12870_2021_3033_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac2c/8162001/c4d75546c042/12870_2021_3033_Fig6_HTML.jpg

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