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Arabidopsis G-protein β subunit AGB1 represses abscisic acid signaling via attenuation of the MPK3-VIP1 phosphorylation cascade

文献类型： 外文期刊

作者： Xu, Dongbei 1 ; Tang, Wensi 1 ; Ma, Yanan 1 ; Wang, Xia 2 ; Yang, Yanzhi 4 ; Wang, Xiaoting 1 ; Xie, Lina 1 ; Huang, Suo 1 ; Qin, Tengfei 1 ; Tang, Weilin 2 ; Xu, Zhaoshi 1 ; Li, Lei 4 ; Tang, Yimiao 3 ; Chen, Ming 1 ; Ma, Youzhi 1 ;

作者机构： 1.Chinese Acad Agr Sci CAAS, Natl Key Facil Crop Gene Resources & Genet Improve, Key Lab Biol & Genet Improvement Triticeae Crops, Minist Agr,Inst Crop Sci, Beijing 100081, Peoples R China

2.Sichuan Agr Univ, Coll Agron, Chengdu 611130, Peoples R China

3.Beijing Acad Agr & Forestry Sci, Inst Hybrid Wheat, Beijing 100097, Peoples R China

4.Peking Univ, Peking Tsinghua Ctr Life Sci, Sch Life Sci, State Key Lab Prot & Plant Gene Res, Beijing 100871, Peoples R China

关键词： Abscisic acid signaling; Arabidopsis; G-protein beta subunit; MPK3; VIP1 transcription factor

期刊名称：JOURNAL OF EXPERIMENTAL BOTANY （ 影响因子：6.9； 五年影响因子：8.0 ）

ISSN： 0022-0957

年卷期： 2024 年 75 卷 5 期

页码：

收录情况： SCI

摘要： Heterotrimeric G proteins play key roles in cellular processes. Although phenotypic analyses of Arabidopsis G beta (AGB1) mutants have implicated G proteins in abscisic acid (ABA) signaling, the AGB1-mediated modules involved in ABA responses remain unclear. We found that a partial AGB1 protein was localized to the nucleus where it interacted with ABA-activated VirE2-interacting protein 1 (VIP1) and mitogen-activated protein kinase 3 (MPK3). AGB1 acts as an upstream negative regulator of VIP1 activity by initiating responses to ABA and drought stress, and VIP1 regulates the ABA signaling pathway in an MPK3-dependent manner in Arabidopsis. AGB1 outcompeted VIP1 for interaction with the C-terminus of MPK3, and prevented phosphorylation of VIP1 by MPK3. Importantly, ABA treatment reduced AGB1 expression in the wild type, but increased in vip1 and mpk3 mutants. VIP1 associates with ABA response elements present in the AGB1 promoter, forming a negative feedback regulatory loop. Thus, our study defines a new mechanism for fine-tuning ABA signaling through the interplay between AGB1 and MPK3-VIP1. Furthermore, it suggests a common G protein mechanism to receive and transduce signals from the external environment.

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