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Abstract
Depletion of the core clock protein BMAL1 in astrocytes leads to disrupted endolysosome function and increased accumulation of organelles.
- Astrocyte-specific deletion of BMAL1 results in a unique activation phenotype that disrupts circadian function.
- In vitro, astrocytes lacking BMAL1 show increased processes like endocytosis and lysosome-dependent protein cleavage.
- Electron microscopy reveals accumulation of autophagosome-like structures in the brains of astrocyte-specific knockout mice.
- Transcriptional analysis indicates a broad dysregulation of lysosome function pathways in astrocytes from both young and aged knockout mice.
- Findings suggest a potential link between neurodegeneration and endolysosome dysfunction related to BMAL1 regulation.
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