ArticleProceedings of the National Academy of Sciences of the United States of America2023
The circadian demethylation of a unique intronic deoxymethylCpG-rich island boosts the transcription of its cognate circadian clock output gene.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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7 citing papers in PubMed.
- Transcriptional remodeling of human skeletal muscle following sleep restriction in postmenopausal women.Physiological genomics · 2026Article
- Targeting the YY1/HDAC2 Transcriptional Axis by Neferine Ameliorates Sleep Deprivation-Induced Cognitive Deficits.Neurochemical research · 2026Article
- Night-shift work is associated with peripheral clock gene dysregulation and circadian transcriptional network remodeling in female healthcare workers.Frontiers in endocrinology · 2026Article
- Long-term DNA methylation changes induced by age and elevated COSkeletal muscle · 2025Article
- Daily rhythm in DNA methylation and the effect of total sleep deprivation.Journal of sleep research · 2025Article
- Signatures of adaptation in myopia-related genes on the sunlight exposure hypothesis.Journal of physiological anthropology · 2023Article
- The HP1α protein is mandatory to repress the circadian clock and its output genes during the 12 h period of transcriptional repression.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
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4 authors.
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Abstract
We demonstrate that there is a tight functional relationship between two highly evolutionary conserved cell processes, i.e., the circadian clock (CC) and the circadian DNA demethylation-methylation of cognate deoxyCpG-rich islands. We have discovered that every circadian clock-controlled output gene (CCG), but not the core clock nor its immediate-output genes, contains a single cognate intronic deoxyCpG-rich island, the demethylation-methylation of which is controlled by the CC. During the transcriptional activation period, these intronic islands are demethylated and, upon dimerization of two YY1 protein binding sites located upstream to the transcriptional enhancer and downstream from the deoxyCpG-rich island, store activating components initially assembled on a cognate active enhancer (a RORE, a D-box or an E-box), in keeping with the generation of a transcriptionally active condensate that boosts the initiation of transcription of their cognate pre-mRNAs. We report how these single intronic deoxyCpG-rich islands are instrumental in such a circadian activation/repression transcriptional process.
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