Cryptochromes mediate rhythmic repression of the glucocorticoid receptor
Open accessAbstract
Mammalian metabolism is highly circadian and major hormonal circuits involving nuclear hormone receptors display interlinked diurnal cycling. However, mechanisms that logically explain the coordination of nuclear hormone receptors and the clock are poorly understood. Here we show that two circadian co-regulators, cryptochromes 1 and 2, interact with the glucocorticoid receptor in a ligand-dependent fashion and globally alter the transcriptional response to glucocorticoids in mouse embryonic fibroblasts: cryptochrome deficiency vastly decreases gene repression and approximately doubles the number of dexamethasone-induced genes, suggesting that cryptochromes broadly oppose glucocorticoid receptor activation and promote repression. In mice, genetic loss of cryptochrome 1 and/or 2 results in glucose intolerance and constitutively high levels of circulating corticosterone, suggesting reduced suppression of the hypothalamic-pituitary-adrenal axis coupled with increased glucocorticoid transactivation in the liver. Genomically, cryptochromes 1 and 2 associate with a glucocorticoid response element in the phosphoenolpyruvate carboxykinase 1 promoter in a hormone-dependent manner, and dexamethasone-induced transcription of the phosphoenolpyruvate carboxykinase 1 gene was strikingly increased in cryptochrome-deficient livers. These results reveal a specific mechanism through which cryptochromes couple the activity of clock and receptor target genes to complex genomic circuits underpinning normal metabolic homeostasis.
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Mice lacking either Cry1 or Cry2 are significantly impaired in restoring normal blood glucose following a glucose injection.
“Even mice lacking either Cry1 (cry1−/−) or Cry2 (cry2−/−) were significantly impaired in their ability to restore normal blood glucose following a glucose injection.”
From Circadian control of glucose metabolism (2014) · cites this paper as [26]
Cry1−/−/Cry2−/− double knockout mice exhibit elevated blood glucose in response to acute feeding after an overnight fast and severely impaired glucose clearance in a glucose tolerance test.
“Cry1−/−/Cry2−/− (double KO) mice exhibit elevated blood glucose in response to acute feeding after an overnight fast and severely impaired glucose clearance in a glucose tolerance test.”
From Circadian control of glucose metabolism (2014) · cites this paper as [26]
Cry-deficient animals are normally responsive to insulin.
“In contrast, Cry-deficient animals were normally responsive to insulin [26].”
From Circadian control of glucose metabolism (2014) · cites this paper as [26]
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- Authors
- Lamia, K. A., Papp, S. J., Yu, R. T., Barish, G. D., Uhlenhaut, N. H., Jonker, J. W., Downes, M., & Evans, R. M.
- Affiliations
- Salk Institute for Biological Studies (US)
- Scripps Research Institute (US)
- Corresponding author
- Lamia, Katja A.
- Evans, Ronald M.
- ORCID
- Venue
- Nature
- Published
- 2011-12
- Volume
- 480
- Issue
- 7378
- Pages
- 552-556
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- PMC
- PMC3245818
- OpenAlex
- W2157959019
- Cited by
- 590
- References
- 29
- Citations by year
- 2026: 23 · 2025: 37 · 2024: 26 · 2023: 46 · 2022: 47 · 2021: 56 · 2020: 48 · 2019: 43 · 2018: 28 · 2017: 35 · 2016: 57 · 2015: 31 · 2014: 46 · 2013: 42 · 2012: 23
- FWCI
- 16.55
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- University of Groningen research database (University of Groningen / Centre for Information Technology) (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- University of Groningen research database (University of Groningen / Centre for Information Technology) (submittedVersion)
- Funders
- Howard Hughes Medical Institute
- Glenn Foundation for Medical Research
- Life Sciences Research Foundation
- National Institutes of Health
- National Cancer Institute (P30CA014195)
- National Institute of Diabetes and Digestive and Kidney Diseases (R37DK057978, K01DK090188, DK090188, DK057978, DK062434, R01DK057978, U19DK062434)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
- Life Sciences › Agricultural and Biological Sciences › Plant Science › Light effects on plants
- Keywords
- cryptochrome, CRY1, CRY2, glucocorticoid receptor, circadian clock, dexamethasone, glucocorticoid response element, PCK1, impaired glucose tolerance, corticosterone, hypothalamic-pituitary-adrenal axis, metabolic homeostasis, mouse embryonic fibroblasts
- MeSH terms
- Animals, Circadian Rhythm, Corticosterone, Dexamethasone, Female, Gene Expression Regulation, Glucocorticoids, Humans, Liver, Phosphoenolpyruvate Carboxykinase (GTP), Receptors, Glucocorticoid, Glucose Intolerance, Mice, Cryptochromes, HEK293 Cells
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