Please use this identifier to cite or link to this item:
Title: The unfolded protein response reverses the effects of glucose on lifespan in chemically-sterilized C. elegans
Authors: Beaudoin-Chabot, Caroline
Wang, Lei
Celik, Cenk
Aishah Tul-Firdaus Abdul Khalid
Thalappilly, Subhash
Xu, Shiyi
Koh, Jhee Hong
Lim, Venus Wen Xuan
Low, Ann Don
Thibault, Guillaume
Keywords: Science::Medicine
Issue Date: 2022
Source: Beaudoin-Chabot, C., Wang, L., Celik, C., Aishah Tul-Firdaus Abdul Khalid, Thalappilly, S., Xu, S., Koh, J. H., Lim, V. W. X., Low, A. D. & Thibault, G. (2022). The unfolded protein response reverses the effects of glucose on lifespan in chemically-sterilized C. elegans. Nature Communications, 13(1), 5889-.
Project: 2018-T2-1-002
Journal: Nature Communications
Abstract: Metabolic diseases often share common traits, including accumulation of unfolded proteins in the endoplasmic reticulum (ER). Upon ER stress, the unfolded protein response (UPR) is activated to limit cellular damage which weakens with age. Here, we show that Caenorhabditis elegans fed a bacterial diet supplemented high glucose at day 5 of adulthood (HGD-5) extends their lifespan, whereas exposed at day 1 (HGD-1) experience shortened longevity. We observed a metabolic shift only in HGD-1, while glucose and infertility synergistically prolonged the lifespan of HGD-5, independently of DAF-16. Notably, we identified that UPR stress sensors ATF-6 and PEK-1 contributed to the longevity of HGD-5 worms, while ire-1 ablation drastically increased HGD-1 lifespan. Together, we postulate that HGD activates the otherwise quiescent UPR in aged worms to overcome ageing-related stress and restore ER homeostasis. In contrast, young animals subjected to HGD provokes unresolved ER stress, conversely leading to a detrimental stress response.
ISSN: 2041-1723
DOI: 10.1038/s41467-022-33630-0
DOI (Related Dataset): 10.21979/N9/GEPEAG
Schools: School of Biological Sciences 
Organisations: Institute of Molecular and Cell Biology, A*STAR
Rights: © 2022 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. The 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 licenses/by/4.0/.
Fulltext Permission: open
Fulltext Availability: With Fulltext
Appears in Collections:SBS Journal Articles

Files in This Item:
File Description SizeFormat 
s41467-022-33630-0.pdf5.74 MBAdobe PDFThumbnail

Citations 50

Updated on Apr 17, 2024

Web of ScienceTM
Citations 50

Updated on Oct 30, 2023

Page view(s)

Updated on Apr 16, 2024

Download(s) 50

Updated on Apr 16, 2024

Google ScholarTM




Items in DR-NTU are protected by copyright, with all rights reserved, unless otherwise indicated.