Overview
- Published in Nature Cell Biology, the Burkewitz-led study shows a progressive age-related loss of ER abundance and complexity using C. elegans with confirmatory data in yeast.
- Genetic tests indicate ER decline occurs independently of unfolded protein response signaling, while blocking core autophagy genes prevents the age-onset ER loss.
- TMEM-131 is identified as an ER-localized factor with a conserved LC3-interacting region that couples ER membranes to autophagosomes and governs selective ER turnover.
- ER remodeling is observed across multiple tissues, including neurons, muscle, intestine, and hypodermis, with yeast showing autophagy-dependent trafficking of ER to the vacuole.
- Diverse lifespan-extending interventions preserve youthful ER architectures, positioning ER-phagy and TMEM-131 as potential therapeutic targets with clinical applications still untested.