Language

English

Publication Date

9-25-2025

Journal

Science

DOI

10.1126/science.adn8754

PMID

40997170

PMCID

PMC12831228

PubMedCentral® Posted Date

1-25-2026

PubMedCentral® Full Text Version

Author MSS

Abstract

The epigenome is sensitive to metabolic inputs and crucial for aging. Lysosomes act as a signaling hub to sense metabolic cues and regulate longevity. We find that lysosomal metabolic pathways signal through the epigenome to regulate transgenerational longevity in Caenorhabditis elegans. Activation of lysosomal lipid signaling and lysosomal adenosine monophosphate-activated protein kinase (AMPK) or reduction of lysosomal mechanistic-target-of-rapamycin (mTOR) signaling increased expression of a histone H3.3 variant and increased its methylation on K79, leading to lifespan extension across multiple generations. This transgenerational pro-longevity effect required intestine-to-germline transportation of histone H3.3 and a germline-specific H3K79 methyltransferase, and was recapitulated by overexpressing H3.3 or the H3K79 methyltransferase. Thus, signals from a lysosome affect the epigenome and link the soma and germline to mediate transgenerational inheritance of longevity.

Keywords

Animals, Longevity, Caenorhabditis elegans, Lysosomes, Histones, Signal Transduction, Epigenome, TOR Serine-Threonine Kinases, Methylation, Caenorhabditis elegans Proteins, Germ Cells, AMP-Activated Protein Kinases, Epigenesis, Genetic, Histone-Lysine N-Methyltransferase

Published Open-Access

yes

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