OSP-1 protects neurons from autophagic cell death induced by acute oxidative stress

Alessandra Donato, Fiona K. Ritchie, Lachlan Lu, Mehershad Wadia, Ramon Martinez-Marmol, Eva Kaulich, Kornraviya Sankorrakul, Hang Lu, Sean Coakley, Elizabeth J. Coulson and Massimo A. Hilliard ()
Additional contact information
Alessandra Donato: The University of Queensland
Fiona K. Ritchie: The University of Queensland
Lachlan Lu: The University of Queensland
Mehershad Wadia: The University of Queensland
Ramon Martinez-Marmol: The University of Queensland
Eva Kaulich: The University of Queensland
Kornraviya Sankorrakul: The University of Queensland
Hang Lu: Georgia Institute of Technology
Sean Coakley: The University of Queensland
Elizabeth J. Coulson: The University of Queensland
Massimo A. Hilliard: The University of Queensland

Nature Communications, 2025, vol. 16, issue 1, 1-19

Abstract: Abstract Oxidative stress, caused by the accumulation of reactive oxygen species (ROS), is a pathological factor in several incurable neurodegenerative conditions as well as in stroke. However, our knowledge of the genetic elements that can be manipulated to protect neurons from oxidative stress-induced cell death is still very limited. Here, using Caenorhabditis elegans as a model system, combined with the optogenetic tool KillerRed to spatially and temporally control ROS generation, we identify a previously uncharacterized gene, oxidative stress protective 1 (osp-1), that protects C. elegans neurons from oxidative damage. Using rodent and human cell cultures, we also show that the protective effect of OSP-1 extends to mammalian cells. Moreover, we demonstrate that OSP-1 functions in a strictly cell-autonomous fashion, and that it localizes to the endoplasmic reticulum (ER) where it has an ER-remodeling function. Finally, we present evidence suggesting that OSP-1 may exert its neuroprotective function by influencing autophagy. Our results point to a potential role of OSP-1 in modulating autophagy, and suggest that overactivation of this cellular process could contribute to neuronal death triggered by oxidative damage.

Date: 2025
References: View references in EconPapers View complete reference list from CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/s41467-024-55105-0 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:16:y:2025:i:1:d:10.1038_s41467-024-55105-0

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/s41467-024-55105-0

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().