har-1/CHCHD10 mutations induce neurodegeneration and mitochondrial fragmentation in Caenorhabditis elegans

2025/04/10 by Audrey Labarre, Ericka Guitard, Gilles Tossing +1
Biochemistry, Genetics and Molecular Biology · #Mitochondrial Function and Pathology

paper · doi:10.17912/micropub.biology.001597

openalex publication_date 2025/04/10 · openalex created_date 2025/06/03 · openalex updated_date 2026/07/28

Abstract

mutants displayed progressive paralysis, degeneration of GABAergic motor neurons, and mitochondrial fragmentation. These strains may be valuable tools for investigating pathogenic mechanisms and therapeutic strategies for neurodegenerative diseases.

Related

• Suppression of har-1/CHCHD10 phenotypes for ALS-FTD therapy discovery
• Reduced Insulin-like signaling restores motor and chemosensory neuron function in C. elegans expressing TDP-43, an ALS-Associated Protein
• cnnm-5 knockdown improves proteostasis of mutant Huntingtin protein in C. elegans
• Depletion of UNK-1 affects head locomotive behaviors in Caenorhabditis elegans
• Programmed cell death throughout life influences the longevity of a defective mitochondrial mutant in C. elegans