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Updated: Feb 10, 2026
Monitoring Cell-autonomous Circadian Clock Rhythms of Gene Expression Using Luciferase Bioluminescence Reporters
Published on: September 27, 2012
Cell-Autonomous and Systemic Circadian Regulation of Gene Expression in Adipocytes
Jennifer M Worthen1, Armina-Lyn M Frederick1, Phillip A Dumesic2
1Department of Molecular and Systems Biology, Geisel School of Medicine at Dartmouth, Hanover, New Hampshire 03755, USA.
The study reveals that 21% of adipocyte genes follow a daily rhythm, impacting energy metabolism and molecular transport. This cell-autonomous clock control in adipocytes offers insights into metabolic disease mechanisms.
Area of Science:
- Cellular biology
- Chronobiology
- Metabolic research
Background:
- Circadian clocks are crucial for adipocyte function.
- Understanding cell-autonomous circadian regulation is key to metabolic disease research.
- Previous studies lacked isolated adipocyte circadian data.
Purpose of the Study:
- To define cell-autonomous circadian programs in adipocytes.
- To identify rhythmic transcripts in adipocytes.
- To compare adipocyte circadian rhythms with in vivo data.
Main Methods:
- Deep RNA sequencing of in vitro-differentiated adipocytes (IVDAs).
- Phase Set Enrichment Analysis (PSEA) to identify rhythmic genes.
- Integration with in vivo adipose tissue datasets.
- Motif enrichment analysis of transcription factors.
Main Results:
- 21% of the adipocyte transcriptome exhibits circadian rhythmicity.
- Intrinsic circadian regulation impacts energy metabolism, transport, and transcription.
- Brown adipose tissue (BAT) and IVDAs show similar rhythmic patterns, distinct from white adipose tissue (eWAT).
- Two distinct temporal regulatory programs (ARNT-family/bHLH-PAS and nuclear receptor-associated) were identified.
Conclusions:
- Novel rhythmic transcripts in adipocytes were identified.
- Cell-autonomous circadian programs in adipocytes were defined.
- Systemic cues further shape adipocyte circadian timing in vivo.
- Findings advance understanding of clock-controlled adipocyte metabolism and metabolic dysfunction.
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