Please use this identifier to cite or link to this item:
|Title:||Membrane phospholipid alteration causes chronic ER stress through early degradation of homeostatic ER-resident proteins||Authors:||Ng, Benjamin S. H.
Shyu Jr., Peter
Seah, Yi Ling
|Issue Date:||2019||Source:||Shyu Jr., P., Ng, B. S. H., Ho, N., Chaw, R., Seah, Y. L., Marvalim, C., & Thibault, G. (2019). Membrane phospholipid alteration causes chronic ER stress through early degradation of homeostatic ER-resident proteins. Scientific Reports, 9(1), 8637-. doi:10.1038/s41598-019-45020-6||Series/Report no.:||Scientific Reports||Abstract:||Phospholipid homeostasis in biological membranes is essential to maintain functions of organelles such as the endoplasmic reticulum. Phospholipid perturbation has been associated to cellular stress responses. However, in most cases, the implication of membrane lipid changes to homeostatic cellular response has not been clearly defined. Previously, we reported that Saccharomyces cerevisiae adapts to lipid bilayer stress by upregulating several protein quality control pathways such as the endoplasmic reticulum-associated degradation (ERAD) pathway and the unfolded protein response (UPR). Surprisingly, we observed certain ER-resident transmembrane proteins, which form part of the UPR programme, to be destabilised under lipid bilayer stress. Among these, the protein translocon subunit Sbh1 was prematurely degraded by membrane stiffening at the ER. Moreover, our findings suggest that the Doa10 complex recognises free Sbh1 that becomes increasingly accessible during lipid bilayer stress, perhaps due to the change in ER membrane properties. Premature removal of key ER-resident transmembrane proteins might be an underlying cause of chronic ER stress as a result of lipid bilayer stress.||URI:||https://hdl.handle.net/10356/89646
|DOI:||http://dx.doi.org/10.1038/s41598-019-45020-6||Rights:||© 2019 The Author(s). This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. Te images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.||Fulltext Permission:||open||Fulltext Availability:||With Fulltext|
|Appears in Collections:||SBS Journal Articles|
Items in DR-NTU are protected by copyright, with all rights reserved, unless otherwise indicated.