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Journal Article

Glucocorticoids Play a Key Role in Circadian Cell Cycle Rhythms

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Dickmeis,  T       
Research Group Zebrafish Chronobiology, Max Planck Institute for Developmental Biology, Max Planck Society;

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Lahiri,  K
Research Group Zebrafish Chronobiology, Max Planck Institute for Developmental Biology, Max Planck Society;

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Vallone,  D       
Research Group Zebrafish Chronobiology, Max Planck Institute for Developmental Biology, Max Planck Society;

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Santoriello,  C
Research Group Zebrafish Chronobiology, Max Planck Institute for Developmental Biology, Max Planck Society;

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Foulkes,  NS       
Research Group Zebrafish Chronobiology, Max Planck Institute for Developmental Biology, Max Planck Society;

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Citation

Dickmeis, T., Lahiri, K., Nica, G., Vallone, D., Santoriello, C., Neumann, C., et al. (2007). Glucocorticoids Play a Key Role in Circadian Cell Cycle Rhythms. PLoS Biology, 5(4): e78. doi:10.1371/journal.pbio.0050078.


Cite as: https://hdl.handle.net/21.11116/0000-000B-8591-A
Abstract
Clock output pathways play a pivotal role by relaying timing information from the circadian clock to a diversity of physiological systems. Both cell-autonomous and systemic mechanisms have been implicated as clock outputs; however, the relative importance and interplay between these mechanisms are poorly understood. The cell cycle represents a highly conserved regulatory target of the circadian timing system. Previously, we have demonstrated that in zebrafish, the circadian clock has the capacity to generate daily rhythms of S phase by a cell-autonomous mechanism in vitro. Here, by studying a panel of zebrafish mutants, we reveal that the pituitary-adrenal axis also plays an essential role in establishing these rhythms in the whole animal. Mutants with a reduction or a complete absence of corticotrope pituitary cells show attenuated cell-proliferation rhythms, whereas expression of circadian clock genes is not affected. We show that the corticotrope deficiency is associated with reduced cortisol levels, implicating glucocorticoids as a component of a systemic signaling pathway required for circadian cell cycle rhythmicity. Strikingly, high-amplitude rhythms can be rescued by exposing mutant larvae to a tonic concentration of a glucocorticoid agonist. Our work suggests that cell-autonomous clock mechanisms are not sufficient to establish circadian cell cycle rhythms at the whole-animal level. Instead, they act in concert with a systemic signaling environment of which glucocorticoids are an essential part.