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Lipid homeostasis is essential for a maximal ER stress response
Lipid homeostasis is essential for a maximal ER stress response
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Length:
20 minutes
Released:
Oct 27, 2022
Format:
Podcast episode
Description
Link to bioRxiv paper:
http://biorxiv.org/cgi/content/short/2022.10.27.513991v1?rss=1
Authors: Garcia, G., Zhang, H., Moreno, S., Tsui, C. K., Webster, B. M., Higuchi-Sanabria, R., Dillin, A.
Abstract:
Changes in lipid metabolism are associated with aging and age-related diseases, including proteopathies. The endoplasmic reticulum (ER) is uniquely a major hub for protein and lipid synthesis, making its function essential for both protein and lipid homeostasis. However, it is less clear how lipid metabolism and protein quality may impact each other. Here, we identity let-767, a putative hydroxysteroid dehydrogenase, as an essential gene for both lipid and ER protein homeostasis. Knockdown of let-767 reduces lipid stores, alters ER morphology in a lipid-dependent manner, and also blocks induction of the Unfolded Protein Response of the ER (UPRER). Interestingly, a global reduction in lipogenic pathways restores UPRER induction in animals with reduced let-767. Specifically, we find that supplementation of 3-oxoacyl, the predicted metabolite directly upstream of let-767, is sufficient to block induction of the UPRER. This study highlights a novel interaction through which changes in lipid metabolism can alter a cell's response to protein-induced stress.
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Podcast created by Paper Player, LLC
http://biorxiv.org/cgi/content/short/2022.10.27.513991v1?rss=1
Authors: Garcia, G., Zhang, H., Moreno, S., Tsui, C. K., Webster, B. M., Higuchi-Sanabria, R., Dillin, A.
Abstract:
Changes in lipid metabolism are associated with aging and age-related diseases, including proteopathies. The endoplasmic reticulum (ER) is uniquely a major hub for protein and lipid synthesis, making its function essential for both protein and lipid homeostasis. However, it is less clear how lipid metabolism and protein quality may impact each other. Here, we identity let-767, a putative hydroxysteroid dehydrogenase, as an essential gene for both lipid and ER protein homeostasis. Knockdown of let-767 reduces lipid stores, alters ER morphology in a lipid-dependent manner, and also blocks induction of the Unfolded Protein Response of the ER (UPRER). Interestingly, a global reduction in lipogenic pathways restores UPRER induction in animals with reduced let-767. Specifically, we find that supplementation of 3-oxoacyl, the predicted metabolite directly upstream of let-767, is sufficient to block induction of the UPRER. This study highlights a novel interaction through which changes in lipid metabolism can alter a cell's response to protein-induced stress.
Copy rights belong to original authors. Visit the link for more info
Podcast created by Paper Player, LLC
Released:
Oct 27, 2022
Format:
Podcast episode
Titles in the series (100)
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