Lysosomes are sites of active metabolism in a cell. They contain various hydrolases that degrade extracellular and intracellular materials during endocytosis and autophagy, respectively. In addition to their long-recognized roles in degradation and recycling, emerging studies have revealed that lysosomes are organizing centers for signal transduction. Lysosome-derived signaling plays crucial roles in regulating nutrient sensing, metabolic adaptation, organelle crosstalk, and aging. In particular, how the degradative role of the lysosome cooperates with its signaling functions to actively modulate lifespan is beginning to be unraveled. This review describes recent advances in the role of the lysosome as a 'signaling hub' that uses three different lysosome-derived signaling pathways to integrate metabolic inputs, organelle interactions, and the control of longevity.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7135937 | PMC |
| http://dx.doi.org/10.1016/j.tcb.2019.08.008 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
NFκB and JNK pathways mediate metabolic adaptation upon ESCRT-I deficiency.
Cell Mol Life Sci
November 2024
Laboratory of Cell Biology, International Institute of Molecular and Cell Biology, Warsaw, Poland.
Endosomal Sorting Complexes Required for Transport (ESCRTs) are crucial for delivering membrane receptors or intracellular organelles for lysosomal degradation which provides the cell with lysosome-derived nutrients. Yet, how ESCRT dysfunction affects cell metabolism remained elusive. To address this, we analyzed transcriptomes of cells lacking TSG101 or VPS28 proteins, components of ESCRT-I subcomplex.
View Article and Find Full Text PDFInteraction between host cell mitochondria and Coxiella burnetii.
Int Rev Cell Mol Biol
June 2023
Department of Microbiology and Immunology, The University of Melbourne at the Peter Doherty Institute for Infection and Immunity, Melbourne, VIC, Australia; Infection and Immunity Program, Monash Biomedicine Discovery Institute and Department of Microbiology, Monash University, Clayton, VIC, Australia. Electronic address:
In order to successfully establish a replicative niche, intracellular bacterial pathogens must influence eukaryotic cell biology. Vesicle and protein traffic, transcription and translation, metabolism and innate immune signaling are all important elements of the host-pathogen interaction that can be manipulated by intracellular bacterial pathogens. The causative agent of Q fever, Coxiella burnetii, is a mammalian adapted pathogen that replicates in a lysosome-derived pathogen-modified vacuole.
View Article and Find Full Text PDFThe endoplasmic reticulum contributes to lysosomal tubulation/sorting driven by LRRK2.
Mol Biol Cell
November 2022
Cell Biology and Gene Expression Section, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892.
Lysosomes are dynamic organelles that can remodel their membrane as an adaptive response to various cell signaling events including membrane damage. Recently, we have discovered that damaged lysosomes form and sort tubules into moving vesicles. We named this process LYTL for LYsosomal Tubulation/sorting driven by LRRK2, as the Parkinson's disease protein LRRK2 promotes tubulation by recruiting the motor adaptor protein JIP4 to lysosomes via phosphorylated RAB proteins.
View Article and Find Full Text PDFEirA Is a Novel Protein Essential for Intracellular Replication of Coxiella burnetii.
Infect Immun
May 2020
Department of Microbiology and Immunology, University of Melbourne at the Peter Doherty Institute for Infection and Immunity, Melbourne, Victoria, Australia
The zoonotic bacterial pathogen is the causative agent of Q fever, a febrile illness which can cause a serious chronic infection. is a unique intracellular bacterium which replicates within host lysosome-derived vacuoles. The ability of to replicate within this normally hostile compartment is dependent on the activity of the Dot/Icm type 4B secretion system.
View Article and Find Full Text PDFExtracellular vesicles released by melanocytes after UVA irradiation promote intercellular signaling via miR21.
Pigment Cell Melanoma Res
July 2020
Experimental Pathology, Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden.
Skin pigmentation is controlled by complex crosstalk between melanocytes and keratinocytes and is primarily induced by exposure to ultraviolet (UV) irradiation. Several aspects of UVA-induced signaling remain to be explored. In skin cells, UVA induces plasma membrane damage, which is repaired by lysosomal exocytosis followed by instant shedding of extracellular vesicles (EVs) from the plasma membrane.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!