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Transcriptomic profiling of subcutaneous white adipose tissue with selective ablation of Bmal1 at ambient and cold condition

ABSTRACT: Mice with beige fat-selective ablation of Bmal1 were generated by crossing Bmal1fl/fl with Prrx1-Cre transgenics. Inguinal subcutaneous adipsoe tissues were collected under ambient temperature at 220C or cold acclimations at 10oC for two weeks.

ORGANISM(S): Mus musculus

PROVIDER: GSE183000 | GEO | 2021/08/31

REPOSITORIES: GEO

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A non-cell autonomous mechanism of beige adipocyte renaissance in subcutaneous adipose tissue

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Transcriptomic profiling of subcutaneous white adipose tissue with selective ablation of Bmal1 at ambient and cold condition

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Proteomics analysis of regulation by Bmal1 and physiological time-restricted feeding

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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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Twenty-four hour rhythms in the absence of the clock gene Bmal1

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