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

© The Author(s) 2023. Published by Oxford University Press on behalf of the Society for Experimental Biology. All rights reserved. For permissions, please email: journals.permissionsoup.com.

Bibliographische Detailangaben
Veröffentlicht in:Journal of experimental botany. - 1985. - 75(2024), 5 vom: 28. Feb., Seite 1615-1632
1. Verfasser: Xu, Dongbei (VerfasserIn)
Weitere Verfasser: Tang, Wensi, Ma, Yanan, Wang, Xia, Yang, Yanzhi, Wang, Xiaoting, Xie, Lina, Huang, Suo, Qin, Tengfei, Tang, Weilin, Xu, Zhaoshi, Li, Lei, Tang, Yimiao, Chen, Ming, Ma, Youzhi
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2024
Zugriff auf das übergeordnete Werk:Journal of experimental botany
Schlagworte:Journal Article Abscisic acid signaling Arabidopsis G-protein β subunit MPK3 VIP1 transcription factor Abscisic Acid 72S9A8J5GW AGB1 protein, Arabidopsis Arabidopsis Proteins mehr... GTP-Binding Protein beta Subunits VIP1 protein, Arabidopsis AtMPK3 protein, Arabidopsis EC 2.7.11.24
Beschreibung
Zusammenfassung:© The Author(s) 2023. Published by Oxford University Press on behalf of the Society for Experimental Biology. All rights reserved. For permissions, please email: journals.permissionsoup.com.
Heterotrimeric G proteins play key roles in cellular processes. Although phenotypic analyses of Arabidopsis Gβ (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
Beschreibung:Date Completed 29.02.2024
Date Revised 29.02.2024
published: Print
Citation Status MEDLINE
ISSN:1460-2431
DOI:10.1093/jxb/erad464