The abstract is read at the publisher; the summary is JClub's.
Increasing PCAF-1 dosage in Caenorhabditis elegans extends lifespan and preserves healthspan by reprogramming stress-responsive transcription through DAF-16/FOXO activation.
- Why it matters: Aging weakens stress sensing and proteome maintenance, but it is unclear whether enhancing a single KAT2 acetyltransferase can strengthen stress programs to protect proteostasis and healthspan.
- What they did: The study increased PCAF-1 dosage in C. elegans and assessed lifespan/healthspan, stress-inducible transcription, proteasomal degradation, and aggregation in neurodegenerative disease models; it also tested conservation and DAF-16 dependence.
- The result: PCAF-1 strengthens inducible stress responses, attenuates age-linked proteasomal decline, and limits protein aggregation while preserving motility and survival; DAF-16 is required for PCAF-1-dependent longevity and protection against polyglutamine aggregation.
The findingWhy it mattersWhat they didThe result
AI summary of the abstract · may contain errors · not medical advice · read the paper.