DVE-1 supports longevity in C. elegans through multiple pathways beyond its known role in mitochondrial stress response. It regulates lifespan independently of the mitochondrial unfolded protein response, influencing dietary restriction, germline signalling, and sensory perception. Its reduced nuclear presence in long-lived mutants suggests a broader cytosolic function in ageing.
November 2024 – Cell Reports
Key takeaways
- DVE-1 extends lifespan through multiple pathways: Traditionally recognised for its role in responding to mitochondrial stress, DVE-1 has now been shown to regulate longevity independently of the mitochondrial unfolded protein response (mitoUPR). This suggests it has a broader function in ageing, influencing lifespan through mechanisms beyond cellular stress adaptation
- Dietary restriction and germline signalling contribute to longevity via DVE-1: DVE-1 plays a critical role in lifespan extension associated with dietary restriction and the loss of reproductive capacity. This indicates that metabolic adaptation and reproductive signalling, both known longevity factors, rely on DVE-1 to exert their beneficial effects on ageing
- Cytosolic DVE-1 may drive ageing benefits: Instead of accumulating in the nucleus, as seen during mitochondrial stress, DVE-1 is found more in the cytosol in long-lived mutants. This shift suggests that its role in lifespan regulation is not limited to gene transcription but may involve previously unrecognised cellular functions that promote longevity
- Longevity pathways may converge on a common mechanism: Sensory perception, dietary restriction, and germline signalling, despite being distinct processes, appear to influence ageing through a shared molecular pathway involving DVE-1. This convergence suggests a central regulatory mechanism that integrates multiple longevity signals to enhance healthspan
Read the article at: Sheng, Yi, et al. “A Mitochondrial Unfolded Protein Response-Independent Role of DVE-1 in Longevity Regulation.” Cell Reports, vol. 43, no. 11, 2024, p. 114889, https://doi.org/10.1016/j.celrep.2024.114889.
