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Lysosome: The metabolic signaling hub

Lamming, Dudley W., Bar‐Peled, Liron·2019·Traffic
DOI 10.1111/tra.12617PMC PMC6294686
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Abstract

For the past five decades, the lysosome has been characterized as an unglamorous cellular recycling center. This notion has undergone a radical shift in the last 10 years, with new research revealing that this organelle serves as a major hub for metabolic signaling pathways. The discovery that master growth regulators, including the protein kinase mTOR (mechanistic target of rapamycin), make their home at the lysosomal surface has generated intense interest in the lysosome's key role in nutrient sensing and cellular homeostasis. The transcriptional networks required for lysosomal maintenance and function are just being unraveled and their connection to lysosome‐based signaling pathways revealed. The catabolic and anabolic pathways that converge on the lysosome connect this organelle with multiple facets of cellular function; when these pathways are deregulated they underlie multiple human diseases, and promote cellular and organismal aging. Thus, understanding how lysosome‐based signaling pathways function will not only illuminate the fascinating biology of this organelle but will also be critical in unlocking its therapeutic potentials.

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  • mTORC1 is regulated by nutrients and hormonal cues, notably amino acids, glucose, oxygen, and cholesterol.

    “mTORC1 is regulated by a wide range of nutrients and hormonal cues, most notably the availability of amino acids, but also glucose, oxygen, and cholesterol 1–3.”

    From Targeting the biology of aging with mTOR inhibitors (2023) · cites this paper as [3]

    In “Metabolic signaling at the lysosomal surface” (page not provided), the paper says mTORC1 integrates hormonal cues and senses amino acids, glucose, and cholesterol; it also emphasizes its sensitivity to amino acids. The paper does not identify oxygen availability as an mTORC1 regulatory cue. A search for oxygen found it only in a reference title about oxygen-glucose deprivation, not in the paper’s account of mTORC1 regulation. (LLM, conf=0.88)

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Metadata

Authors
Lamming, D. W., & Bar‐Peled, L.
Affiliations
  • William S. Middleton Memorial Veterans Hospital Madison Wisconsin
  • Department of Molecular Medicine The Scripps Research Institute La Jolla California
ORCID
Venue
Traffic
Publisher
Wiley
Published
2018-11-14
Volume
20
Issue
1
Pages
27-38
ISSN
  • 1398-9219
  • 1600-0854
DOI
10.1111/tra.12617
PMC
PMC6294686
Cited by
173
References
43
Language
en
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Funders
  • Diabetes Research Center, University of Washington (2 P30 DK020579)
  • National Institutes of Health (AG050135, AG051974, AG056771, CA215249)
  • U.S. Department of Veterans Affairs (I01‐BX004031)
  • Damon Runyon Cancer Research Foundation (DRG‐2178‐14)
  • American Federation for Aging Research

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