Glycogen synthase is required for heat shock-mediated autophagy induction in neuronal cells
Year: 2025
Type: article
Abstract: Autophagy is an essential cellular process that facilitates the degradation of aggregated proteins and damaged organelles to maintain cellular homeostasis and promote cell survival. Recent studies have indicated a direct role for glycogen synthase (GS) in activating neuronal autophagy and in conferring protection against cytotoxic misfolded proteins. Since heat shock induces protein misfolding and autophagy is an essential component of the heat shock response that clears the misfolded proteins, we looked at the possible role of GS in heat shock response pathways in neuronal cells. We demonstrate an increase in the activity and level of GS and a concomitant increase in the glycogen level during the heat shock and post-heat shock recovery period. These changes had a direct correlation with autophagy induction. We further demonstrate that heat shock transcription factor 1 regulates the level and activation of GS during heat shock and that GS is essential for the induction of autophagy during heat stress in neuronal cells. Intriguingly, the partial knock-down of GS led to increased death due to heat shock in neuronal cells and Drosophila. Our study offers a novel insight into the role of GS and glycogen metabolic pathways in heat shock response in neuronal cells.
Source: Biology Open
DOI: 10.1242/bio.061605
Authors: Pratibha Bhadauriya, Akanksha Onkar, Kamali Nagarajan, Kavikumar Angamuthu Karuppusamy, Subramaniam Ganesh, Saloni Agarwal
Institution: Indian Institute of Technology Kanpur
Language: English
Subfield: Epidemiology
Field: Medicine
Domain: Health Sciences
Open Access status: gold
Estimated APC paid: $1,995
Funders: Institute for Research in Biomedicine, Indian Institute of Technology Kanpur, Department of Science and Technology, Ministry of Science and Technology, India, Indian Council of Medical Research, Ministry of Health and Family Welfare, University of Texas at Dallas, Science and Engineering Research Board
OpenAlex ID: W4407189195
