TickingClock的个人博客分享 http://blog.sciencenet.cn/u/TickingClock

博文

Plant Physiology:SIB1和LSD1蛋白拮抗调控GLK1/2,调节光合相关核基因

已有 2269 次阅读 2022-1-1 23:46 |个人分类:一周精读|系统分类:论文交流

Antagonistic modules regulate photosynthesis-associated nuclear genes via GOLDEN2-LIKE transcription factors

第一作者Mengping Li

第一单位中科院分子植物科学卓越中心

第一通讯Chanhong Kim


 Abstract 


背景回顾GOLDEN2-LIKE (GLK) transcription factors drive the expression of photosynthesis-associated nuclear genes (PhANGs) indispensable for chloroplast biogenesis. Salicylic acid (SA)-induced SIGMA FACTOR-BINDING PROTEIN 1 (SIB1), a transcription coregulator and positive regulator of cell death, interacts with GLK1 and GLK2 to reinforce the expression of PhANGs, leading to photoinhibition of photosystem II and singlet oxygen (1O2) burst in chloroplasts. 1O2 then contributes to SA-induced cell death via EXECUTER 1 (EX11O2 sensor protein)-mediated retrograde signaling upon reaching a critical level. 


研究问题This earlier finding has initiated research on the potential role of GLK1/2 and EX1 inSA signaling


主要发现:Consistent with this view, we reveal that LESION-SIMULATING DISEASE 1 (LSD1), a transcription coregulator and negative regulator of SA-primed cell death, interacts with GLK1/2 to repress their activities in Arabidopsis (Arabidopsis thaliana). 


结果1-过表达和功能缺失:Overexpression of LSD1 repressed GLK target genes, including PhANGs, whereas loss of LSD1 enhanced their expression. Remarkably, LSD1 overexpression inhibited chloroplast biogenesis, resembling the characteristic glk1glk2 double mutant phenotype. 


结果2-LSD1-GLK:Subsequent chromatin immunoprecipitation coupled with expression analyses further revealed that LSD1 inhibits the DNA-binding activity of GLK1 towards its target promoters. 


结果3-SIB1与LSD1拮抗:SA-induced nuclear-targeted SIB1 proteins appeared to interrupt the LSD1-GLK interaction, and the subsequent SIB1-GLK interaction activated EX1-mediated 1O2 signaling, elucidating antagonistic modules SIB1 and LSD1 in the regulation of GLK activity. 


结论:Taken together, we provide a working model that SIB1 and LSD1, mutually exclusive SA-signaling components, antagonistically regulate GLK1/2 to fine-tune the expression of PhANGs, thereby modulating 1Ohomeostasis and related stress responses.


7.jpg


 摘 要 


GLK转录因子驱动光合相关核基因(PhANGs)的表达,对于叶绿体的发育是不可或缺的。受水杨酸诱导的转录共调控子SIB1正调控细胞死亡,该基因能够与GLK1/2发生互作,从而增强PhANGs的表达,导致光系统II的光抑制以及叶绿体中的单态氧爆发。接着,单态氧通过单态氧感知蛋白EX1介导的逆行信号作用于水杨酸诱导的细胞死亡。这些发现开启了对于GLK1/2和EX1在水杨酸信号转导功能方面的研究。与此一致,作者发现在拟南芥中,转录共调控因子、水杨酸诱导的细胞死亡的正调控因子LSD1能够与GLK1/2互作,抑制GLK1/2的活性。过表达LSD1会抑制PhANGsGLK靶向基因的表达,而LSD1的功能缺失会增强这些基因的表达。重要的是,LSD1过表达会抑制叶绿体生物发生,这与glk1glk2双突的表型缺陷类似。后续的染色质免疫共沉淀和表达分析表明,LSD1抑制了GLK1蛋白结合到靶标基因启动子上的DNA结合活性。水杨酸诱导的核靶向SIB1蛋白能够扰乱LSD1-GLK的互作,随后SIB1-GLK互作激活了EX1介导的单态氧信号转导,表明SIB1和LSD1蛋白在GLK活性调控方面存在拮抗作用。综上,本文的研究揭示了互不相容的水杨酸信号转导组分SIB1和LSD1蛋白拮抗调控GLK1/2,从而精细调控PhANGs的表达,最终调节单态氧的内稳态及相关的胁迫响应。


 通讯作者 

** Chanhong Kim **


个人简介:

1988-1998年,韩国东国大学,学士/硕士;

2000-2004年,苏黎世联邦理工学院,博士;

2004-2006年,苏黎世联邦理工学院,博后;

2006-2008年,苏黎世联邦理工学院,研究组长;

2008-2014年,康奈尔大学-鲍依斯•汤普森植物研究所,研究员;

2014年-至今,中科院上海植物逆境生物学研究中心,研究员。


研究方向光合作用与胁迫信号。


doi: https://doi.org/10.1093/plphys/kiab600


Journal: Plant Physiology

Published dateDecember 24, 2021



https://m.sciencenet.cn/blog-3158122-1319206.html

上一篇:PNAS:THESEUS1调控拟南芥细胞壁强度与ABA生成
下一篇:the plant journal:两个槭树(梣叶槭、糖槭)基因组

0

该博文允许注册用户评论 请点击登录 评论 (0 个评论)

数据加载中...

Archiver|手机版|科学网 ( 京ICP备07017567号-12 )

GMT+8, 2024-4-23 19:51

Powered by ScienceNet.cn

Copyright © 2007- 中国科学报社

返回顶部