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拟南芥外切核糖核酸酶USB1与PPR结构域蛋白SOAR1相互作用,负向调控脱落酸信号传导。

Arabidopsis exoribonuclease USB1 interacts with the PPR-domain protein SOAR1 to negatively regulate abscisic acid signaling.

作者信息

Ma Yu, Zhang Shang, Bi Chao, Mei Chao, Jiang Shang-Chuan, Wang Xiao-Fang, Lu Zhi John, Zhang Da-Peng

机构信息

MOE Key Lab of Bioinformatics, Center for Plant Biology, School of Life Sciences,Tsinghua University, Beijing, China.

出版信息

J Exp Bot. 2020 Oct 7;71(19):5837-5851. doi: 10.1093/jxb/eraa315.

DOI:10.1093/jxb/eraa315
PMID:32969475
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7541913/
Abstract

Signaling by the phytohormone abscisic acid (ABA) involves pre-mRNA splicing, a key process of post-transcriptional regulation of gene expression. However, the regulatory mechanism of alternative pre-mRNA splicing in ABA signaling remains largely unknown. We previously identified a pentatricopeptide repeat protein SOAR1 (suppressor of the ABAR-overexpressor 1) as a crucial player downstream of ABAR (putative ABA receptor) in ABA signaling. In this study, we identified a SOAR1 interaction partner USB1, which is an exoribonuclease catalyzing U6 production for spliceosome assembly. We reveal that together USB1 and SOAR1 negatively regulate ABA signaling in early seedling development. USB1 and SOAR1 are both required for the splicing of transcripts of numerous genes, including those involved in ABA signaling pathways, suggesting that USB1 and SOAR1 collaborate to regulate ABA signaling by affecting spliceosome assembly. These findings provide important new insights into the mechanistic control of alternative pre-mRNA splicing in the regulation of ABA-mediated plant responses to environmental cues.

摘要

植物激素脱落酸(ABA)信号传导涉及前体mRNA剪接,这是基因表达转录后调控的关键过程。然而,ABA信号传导中可变前体mRNA剪接的调控机制仍 largely未知。我们之前鉴定出一个五肽重复蛋白SOAR1(ABAR过表达抑制因子1),它是ABA信号传导中ABAR(假定的ABA受体)下游的关键因子。在本研究中,我们鉴定出一个SOAR1相互作用蛋白USB1,它是一种外切核糖核酸酶,催化用于剪接体组装的U6生成。我们发现USB1和SOAR1共同在幼苗早期发育中负向调控ABA信号传导。USB1和SOAR1对于众多基因转录本的剪接都是必需的,包括那些参与ABA信号通路的基因,这表明USB1和SOAR1通过影响剪接体组装协同调控ABA信号传导。这些发现为ABA介导的植物对环境信号响应调控中可变前体mRNA剪接的机制控制提供了重要的新见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef67/7541913/f5088f7fd841/eraa315_fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef67/7541913/b67841cbb29d/eraa315_fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef67/7541913/0bcf75e5f820/eraa315_fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef67/7541913/15290bf01682/eraa315_fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef67/7541913/2440e1e7ecc2/eraa315_fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef67/7541913/f5088f7fd841/eraa315_fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef67/7541913/b67841cbb29d/eraa315_fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef67/7541913/0bcf75e5f820/eraa315_fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef67/7541913/15290bf01682/eraa315_fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef67/7541913/2440e1e7ecc2/eraa315_fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef67/7541913/f5088f7fd841/eraa315_fig5.jpg

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两个猕猴桃物种五重基序重复蛋白基因家族的全基因组分析,重点关注 RNA 编辑在病原体胁迫中的作用。
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