Exploring the organismal role of UFMylation in development, stress resilience and neurological function in C. elegans - PubMed
3 hours ago
- #C. elegans
- #neurodegeneration
- #UFMylation
- UFMylation involves conjugating UFM1 to proteins, regulating ribosomal homeostasis, ER stress response, and DNA repair.
- In C. elegans, UFM-1 expression increases from larval stages to adulthood, mainly in intestinal cells, and is upregulated during ER stress and autophagy.
- UFMylation is crucial for lifespan, development, and reproduction, with mutants showing increased gonadal dysfunction and sterility.
- Loss of ufm-1 enhances stress tolerance, possibly due to a hormetic response to persistent ER stress, and activates the ER unfolded protein response.
- UFM-1 loss exacerbates proteotoxicity, accelerating paralysis and increasing amyloid-β, α-synuclein, and polyQ aggregates in muscle-expressed models.
- Mutants exhibit impaired locomotion, altered swimming patterns similar to aging worms, and accelerated sensory neuron dysfunction and neurodegeneration.