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Summary
Lysosomes were discovered more than 60 years ago as highly acidic cellular organelles containing many enzymes responsible for breaking down macromolecules (1). Since then, their roles have expanded. Lysosomes function in autophagy, the process that breaks down cellular components to allow cell survival and homeostasis in the face of starvation (1). These organelles also have emerged as a signaling hub for the enzyme mechanistic target of rapamycin (mTOR), a protein kinase involved in cellular and organismal growth responses to nutrient availability (2). We also now recognize links between aberrant lysosomal function and several diseases, including lysosomal storage diseases (e.g., Tay-Sachs disease) and neurodegenerative disorders (e.g., Parkinson's disease), and also with aging (1). On page 83 of this issue, Folick et al. (3) indicate how lysosomes play a role in the latter—by deploying a lipid molecule to the nucleus, whose impact on gene expression extends life span in an animal model (the nematode Caenorhabditis elegans). The study not only uncovers a lysosome-to-nucleus signaling pathway but also highlights the potential of lipids in mediating long-range physiological effects.
