Plant G proteins interact with endoplasmic reticulum luminal protein receptors to regulate endoplasmic reticulum retrieval

• Published in: Journal of integrative plant biology 2018-07, Vol.60 (7), p.541-561
• Main Authors: Wang, Shanshan, Xie, Ke, Xu, Guoyong, Zhou, Huarui, Guo, Qiang, Wu, Jingyi, Liao, Zengwei, Liu, Na, Wang, Yan, Liu, Yule
• Format: Article
• Language: English
• Subjects: Binding sites; Biomolecules; Cloning, Molecular; Endoplasmic reticulum; Endoplasmic Reticulum - metabolism; Gene Silencing; Golgi apparatus; Golgi Apparatus - metabolism; Green Fluorescent Proteins - metabolism; GTP-Binding Proteins - metabolism; Homeostasis; Nicotiana - metabolism; Plant Proteins - metabolism; Protein Binding; Protein Multimerization; Protein Subunits - metabolism; Proteins; Receptor mechanisms; Receptors; Retrieval; Retrograde transport
• ISSN: 1672-9072; 1744-7909
• DOI: 10.1111/jipb.12648

Maintaining endoplasmic reticulum (ER) homeostasis is essential for the production of biomolecules. ER retrieval, i.e., the retrograde transport of compounds from the Golgi to the ER, is one of the pathways that ensures ER homeostasis. However, the mechanisms underlying the regulation of ER retrieval in plants remain largely unknown. Plant ERD2‐like proteins (ERD2s) were recently suggested to function as ER luminal protein receptors that mediate ER retrieval. Here, we demonstrate that heterotrimeric G protein signaling is involved in ERD2‐mediated ER retrieval. We show that ERD2s interact with the heterotrimeric G protein Gα and Gγ subunits at the Golgi. Silencing of Gα, Gβ, or Gγ increased the retention of ER luminal proteins. Furthermore, overexpression of Gα, Gβ, or Gγ caused ER luminal proteins to escape from the ER, as did the co‐silencing of ERD2a and ERD2b. These results suggest that G proteins interact with ER luminal protein receptors to regulate ER retrieval. G proteins have multiple roles inside the cells. In this study, we found a new function of heterotrimeric G proteins. We demonstrated that G protein subunits negatively regulate the ER retrieval by interacting with ER luminal protein receptors, which is responsible for ER retrieval from Golgi to ER.