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三聚体 G 蛋白介导的信号转导参与应激介导的生长抑制。

Heterotrimeric G Protein-Mediated Signaling Is Involved in Stress-Mediated Growth Inhibition in .

机构信息

Department of Biotechnology, Duksung Women's University, Seoul 03169, Republic of Korea.

出版信息

Int J Mol Sci. 2023 Jul 3;24(13):11027. doi: 10.3390/ijms241311027.

DOI:10.3390/ijms241311027
PMID:37446209
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10342085/
Abstract

Heterotrimeric G protein-mediated signaling plays a vital role in physiological and developmental processes in eukaryotes. On the other hand, because of the absence of a G protein-coupled receptor and self-activating mechanism of the Gα subunit, plants appear to have different regulatory mechanisms, which remain to be elucidated, compared to canonical G protein signaling established in animals. Here we report that heterotrimeric G protein subunits, such as Gα () and Gβ (), regulate plant growth under stress conditions through the analysis of heterotrimeric G protein mutants. Flg22-mediated growth inhibition in wild-type roots was found to be caused by a defect in the elongation zone, which was partially blocked in but not . These results suggest that may negatively regulate plant growth under biotic stress conditions. In addition, and exhibited genetically opposite effects on -mediated growth inhibition under heat stress conditions. Therefore, these results suggest that plant G protein signaling is probably related to stress-mediated growth regulation for developmental plasticity in response to biotic and abiotic stress conditions.

摘要

异三聚体 G 蛋白介导的信号转导在真核生物的生理和发育过程中起着至关重要的作用。另一方面,由于植物缺乏 G 蛋白偶联受体和 Gα 亚基的自我激活机制,与在动物中建立的经典 G 蛋白信号相比,其调控机制尚待阐明。在这里,我们通过分析异三聚体 G 蛋白突变体报告说,异三聚体 G 蛋白亚基(如 Gα()和 Gβ())通过调控植物在胁迫条件下的生长。我们发现,Flg22 介导的野生型根生长抑制是由于伸长区缺陷引起的,而在突变体中部分受阻,但在 突变体中不受影响。这些结果表明,在生物胁迫条件下,可能负调控植物的生长。此外,和在热胁迫条件下对介导的生长抑制表现出遗传上相反的影响。因此,这些结果表明,植物 G 蛋白信号转导可能与胁迫介导的生长调节有关,以响应生物和非生物胁迫条件下的发育可塑性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bae1/10342085/789366a4eb2c/ijms-24-11027-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bae1/10342085/d98396942210/ijms-24-11027-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bae1/10342085/f95dce530de9/ijms-24-11027-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bae1/10342085/479f3513cab9/ijms-24-11027-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bae1/10342085/01576730ffba/ijms-24-11027-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bae1/10342085/14f24b578e6d/ijms-24-11027-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bae1/10342085/789366a4eb2c/ijms-24-11027-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bae1/10342085/d98396942210/ijms-24-11027-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bae1/10342085/f95dce530de9/ijms-24-11027-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bae1/10342085/479f3513cab9/ijms-24-11027-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bae1/10342085/01576730ffba/ijms-24-11027-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bae1/10342085/14f24b578e6d/ijms-24-11027-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bae1/10342085/789366a4eb2c/ijms-24-11027-g006.jpg

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