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The role of core circadian component BMAL1 or CLOCK in human bone marrow mesenchymal stem cells osteogenic capacity

ABSTRACT: To elucidate how the core circadian component BMAL1 and clock regulate the osteogenic capacity of human bone marrow MSCs, RNA-seq was performed to study the impact of diminishing core component BMAL1 or CLOCK in MSCs by lentiviruses.

ORGANISM(S): Homo sapiens

PROVIDER: GSE208729 | GEO | 2022/07/26

REPOSITORIES: GEO

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BMAL1 associates with NOP58 in the nucleolus and contributes to pre-rRNA processing

Project description:The transcription factor BMAL1 is a core element of the circadian clock that contributes to cyclic control of genes transcribed by RNA polymerase II. By using biochemical cellular fractionation and immunofluorescence analyses we reveal a previously uncharacterized nucleolar localization for BMAL1. We used an unbiased approach to determine the BMAL1 interactome by mass spectrometry and identified NOP58 as a prominent nucleolar interactor. NOP58, a core component of the box C/D small nucleolar ribonucleoprotein complex, associates with Snord118 to control specific pre-ribosomal RNA (rRNA) processing steps. These results suggest a non-canonical role of BMAL1 in rRNA regulation. Indeed, we show that BMAL1 controls NOP58-associated Snord118 nucleolar levels and cleavage of unique pre-rRNA intermediates. Our findings identify an unsuspected function of BMAL1 in the nucleolus that appears distinct from its canonical role in the circadian clock system

2020-08-25 | PXD018946 | Pride

The role of core circadian component BMAL1 or CLOCK in human bone marrow mesenchymal stem cells osteogenic capacity

Project description:The role of core circadian component BMAL1 or CLOCK in human bone marrow mesenchymal stem cells osteogenic capacity

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Circadian key component CLOCK/BMAL1 interferes with segmentation clock in mouse embryonic organoids

Project description:In mammals, circadian clocks are strictly suppressed during early embryonic stages as well as pluripotent stem cells, by the lack of CLOCK/BMAL1 mediated circadian feedback loops. During ontogenesis, the innate circadian clocks emerge gradually at a late developmental stage, then, with which the circadian temporal order is invested in each cell level throughout a body. Meanwhile, in the early developmental stage, a segmented body plan is essential for an intact developmental process and somitogenesis is controlled by another cell-autonomous oscillator, the segmentation clock, in the posterior presomitic mesoderm (PSM). In the present study, focusing upon the interaction between circadian key components and the segmentation clock, we investigated the effect of the CLOCK/BMAL1 on the segmentation clock Hes7 oscillation, revealing that the expression of functional CLOCK/BMAL1 severely interferes with the ultradian rhythm of segmentation clock in induced PSM and gastruloids. RNA sequencing analysis showed that the premature expression of CLOCK/BMAL1 affects the Hes7 transcription and its regulatory pathways. These results suggest that the suppression of CLOCK/BMAL1-mediated transcriptional regulation during the somitogenesis may be inevitable for intact mammalian development.

2021-12-09 | GSE181295 | GEO

Circadian key component CLOCK/BMAL1 interferes with segmentation clock in mouse embryonic organoids

Project description:Circadian key component CLOCK/BMAL1 interferes with segmentation clock in mouse embryonic organoids

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The clock gene BMAL1 inhibits macrophage motility, phagocytosis, and impairs defence against pneumonia

Project description:The circadian clock regulates many aspects of immunity. Bacterial infections are affected by time of day, but the mechanisms involved remain undefined. Here we show that loss of the core clock protein BMAL1 in macrophages confers protection against pneumococcal pneumonia. RNAseq was performed on peritoneal macrophages from wild type and BMAL1 knock out mice.

2019-12-20 | E-MTAB-8411 | biostudies-arrayexpress

BMAL1-TTK-H2Bub1 loop deficiency contributes to impaired BM-MSC-mediated bone formation in senile osteoporosis

Project description:We performed multiomic high-throughput sequencing to recapitulated the BMAL1-H2Bub1 loop in mesenchymal stem cells osteogenesis. We used lentiviruses to diminish RNF40 and WAC, which are parts of the obligate complex and monoubiquitinated histone H2B, in MSCs, and analysed the H2Bub1 and PolII CUT&Tag-seq.

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LC-MS/MS identification of BMAL1 interaction proteins

Project description:Advances in circadian research revealed an intricate relationship between aging and circadian rhythms. However, whether and how the circadian machinery contribute to stem cell aging, especially in primates, remains poorly understood. In this study, we investigated the role of BMAL1, the only non-redundant circadian clock component, during aging in mesenchymal progenitor cells (MPCs). We observed an accelerated aging phenotype in both BMAL1 deficient human and cynomolgus monkey MPCs. Notably, this phenotype is mainly attributed to a transcriptional-independent role of BMAL1 in stabilizing the heterochromatin and thus preventing LINE1 activation. In senescent MPCs from human and cynomolgus monkeys, dampened LINE1 binding capacity of BMAL1 and synergistically activated LINE1 transcripts were observed. Furthermore, similar de-stabilized heterochromatin and aberrant LINE1s transcription was observed in the skin and muscle tissues from BMAL1-deficient cynomolgus monkey. Altogether, these findings uncover a noncanonical role of BMAL1 in stabilizing heterochromatin to inactivate LINE1 that drives aging in primates.

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Microglial gene expression in Bmal1 cKO and WT mice

Project description:To investigate the interaction between aging and microglial circadian rhythmicity, we examined mice deficient in the core clock transcription factor, BMAL1, in microglia.

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Genome-wide binding of Bmal1 and Clock in adult mouse skeletal muscle.

Project description:The goal of this study was to define the binding sites of the core circadian factors, BMAL1 and CLOCK across the genome in adult mouse skeletal muscle. We found that mitochondrial inner-membrane genes were among the most enriched rhythmic genes via gene ontology analysis, and ChIP-Seq analysis corroborated the role of Clock and Bmal1 in targeting promoters of mitochondrial inner-membrane genes.

2021-08-12 | GSE143334 | GEO

Neuronal deletion of the circadian clock gene Bmal1 induces cell-autonomous dopaminergic neurodegeneration

Project description:Circadian rhythm dysfunction is a hallmark of Parkinson Disease (PD), and diminished expression of the core clock gene Bmal1 has been described in PD patients. BMAL1 is required for core circadian clock function, but also serves non-rhythmic functions. Germline Bmal1 deletion can cause brain oxidative stress and synapse loss in mice, and can exacerbate dopaminergic neurodegeneration in response to MPTP. Here we examined the impact of cell type-specific Bmal1 deletion on dopaminergic neuron viability in vivo. We observed that global, post-natal deletion of Bmal1 caused spontaneous loss of tyrosine hydroxylase-positive (TH+) dopaminergic neurons in the substantia nigra pars compacta (SNpc). This was not due to disruption of behavioral circadian rhythms, and was not induced by astrocyte- or microglia-specific Bmal1 deletion. However, either pan-neuronal or TH neuron-specific Bmal1 deletion caused cell-autonomous loss of TH+ neurons in the SNpc. Finally, global Bmal1 deletion exacerbated TH+ neuron loss following injection of alpha-synclein fibrils. Transcriptomic analysis of neuron-specific Bmal1 KO brain revealed dysregulation of pathways involved in oxidative phosphorylation and Parkinson Disease.

2023-08-18 | GSE241200 | GEO

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