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Abstract
Lack of γ or α expression in mice resulted in a significant reduction in peak expression levels of clock genes such as Cry1, Bmal1, and Per2.
- RORγ and RORα showed redundancy in regulating clock gene expression in certain tissues.
- RORγ can activate reporter gene activity by binding to regulatory regions of clock genes.
- Co-expression of Rev-Erbα or a ROR antagonist can repress RORγ's activation of these genes.
- RORγ regulates clock genes directly in a time-dependent manner, as shown by DNA binding studies.
- Changes in histone acetylation and chromatin accessibility are associated with ROR-mediated transcriptional activation.
- The rhythmic expression of Avpr1a in the liver is linked to RORγ, suggesting its role in linking circadian rhythms to metabolic gene regulation.
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