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REV-ERBα mediates complement expression and diurnal regulation of microglial synaptic phagocytosis
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REV-ERBα mediates complement expression and diurnal regulation of microglial synaptic phagocytosis
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REV-ERBα mediates complement expression and diurnal regulation of microglial synaptic phagocytosis
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Journal Article
REV-ERBα mediates complement expression and diurnal regulation of microglial synaptic phagocytosis
2020
Overview
The circadian clock regulates various aspects of brain health including microglial and astrocyte activation. Here, we report that deletion of the master clock protein BMAL1 in mice robustly increases expression of complement genes, including C4b and C3 , in the hippocampus. BMAL1 regulates expression of the transcriptional repressor REV-ERBα, and deletion of REV-ERBα causes increased expression of C4b transcript in neurons and astrocytes as well as C3 protein primarily in astrocytes. REV-ERBα deletion increased microglial phagocytosis of synapses and synapse loss in the CA3 region of the hippocampus. Finally, we observed diurnal variation in the degree of microglial synaptic phagocytosis which was antiphase to REV-ERBα expression. This daily variation in microglial synaptic phagocytosis was abrogated by global REV-ERBα deletion, which caused persistently elevated synaptic phagocytosis. This work uncovers the BMAL1-REV-ERBα axis as a regulator of complement expression and synaptic phagocytosis in the brain, linking circadian proteins to synaptic regulation.
Publisher
eLife Sciences Publications, Ltd,eLife Sciences Publications Ltd
Subject
/ ARNTL Transcription Factors - deficiency
/ ARNTL Transcription Factors - genetics
/ CA3 Region, Hippocampal - cytology
/ CA3 Region, Hippocampal - metabolism
/ Complement System Proteins - genetics
/ Complement System Proteins - metabolism
/ Female
/ Male
/ Nuclear Receptor Subfamily 1, Group D, Member 1 - deficiency
/ Nuclear Receptor Subfamily 1, Group D, Member 1 - genetics
/ Nuclear Receptor Subfamily 1, Group D, Member 1 - metabolism
