biostudies-literatureMcKee CANCATS NIH HHSNIA NIH HHSNCI NIH HHSHHS | NIH | National Institute on AgingNIH HHSe2220551120https://www.ebi.ac.uk/biostudies/studies/S-EPMC10194014biostudies-literatureUnknown120(20)An emerging role for the circadian clock in autophagy and lysosome function has opened new avenues for exploration in the field of neurodegeneration. The daily rhythms of circadian clock proteins may coordinate gene expression programs involved not only in daily rhythms but in many cellular processes. In the brain, astrocytes are critical for sensing and responding to extracellular cues to support neurons. The core clock protein BMAL1 serves as the primary positive circadian transcriptional regulator and its depletion in astrocytes not only disrupts circadian function but also leads to a unique cell-autonomous activation phenotype. We report here that astrocyte-specific deletion of <i>Bmal1</i> influences endolysosome function, autophagy, and protein degradation dynamics. In vitro, <i>BmalProceedings of the National Academy of Sciences of the United States of AmericaCircadian clock protein BMAL1 broadly influences autophagy and endolysosomal function in astrocytes.PMC10194014P30 CA091842UL1 TR002345S10 OD032186R01AG054517R01 AG054517RF1 AG061776Musiek ESMcKee CAPolino AJKing MWfalseCircadian clock protein BMAL1 broadly influences autophagy and endolysosomal function in astrocytes.An emerging role for the circadian clock in autophagy and lysosome function has opened new avenues for exploration in the field of neurodegeneration. The daily rhythms of circadian clock proteins may coordinate gene expression programs involved not only in daily rhythms but in many cellular processes. In the brain, astrocytes are critical for sensing and responding to extracellular cues to support neurons. The core clock protein BMAL1 serves as the primary positive circadian transcriptional regulator and its depletion in astrocytes not only disrupts circadian function but also leads to a unique cell-autonomous activation phenotype. We report here that astrocyte-specific deletion of <i>Bmal1</i> influences endolysosome function, autophagy, and protein degradation dynamics. In vitro, <i>Bmal2023-01-01T00:00:00Z2023 May2026-05-28T22:28:18.131Z2025-04-06T08:03:49.063ZS-EPMC101940143715583910.1073/pnas.2220551120