Circadian clock mechanism driving mammalian photoperiodism

S. H. Wood, M. M. Hindle, Y. Mizoro, Y. Cheng, B. R. C. Saer, K. Miedzinska, H. C. Christian, N. Begley, J. McNeilly, A. S. McNeilly, S. L. Meddle, D. W. Burt and A. S. I. Loudon ()
Additional contact information
S. H. Wood: University of Manchester
M. M. Hindle: The Roslin Institute, and Royal (Dick) School of Veterinary Studies University of Edinburgh
Y. Mizoro: University of Manchester
Y. Cheng: The University of Queensland
B. R. C. Saer: University of Manchester
K. Miedzinska: The Roslin Institute, and Royal (Dick) School of Veterinary Studies University of Edinburgh
H. C. Christian: University of Oxford, Department of Physiology, Anatomy and Genetics, Le Gros Clark Building
N. Begley: University of Manchester
J. McNeilly: MRC Centre for Reproductive Health, Queen’s Medical Research Institute
A. S. McNeilly: MRC Centre for Reproductive Health, Queen’s Medical Research Institute
S. L. Meddle: The Roslin Institute, and Royal (Dick) School of Veterinary Studies University of Edinburgh
D. W. Burt: The Roslin Institute, and Royal (Dick) School of Veterinary Studies University of Edinburgh
A. S. I. Loudon: University of Manchester

Nature Communications, 2020, vol. 11, issue 1, 1-15

Abstract: Abstract The annual photoperiod cycle provides the critical environmental cue synchronizing rhythms of life in seasonal habitats. In 1936, Bünning proposed a circadian-based coincidence timer for photoperiodic synchronization in plants. Formal studies support the universality of this so-called coincidence timer, but we lack understanding of the mechanisms involved. Here we show in mammals that long photoperiods induce the circadian transcription factor BMAL2, in the pars tuberalis of the pituitary, and triggers summer biology through the eyes absent/thyrotrophin (EYA3/TSH) pathway. Conversely, long-duration melatonin signals on short photoperiods induce circadian repressors including DEC1, suppressing BMAL2 and the EYA3/TSH pathway, triggering winter biology. These actions are associated with progressive genome-wide changes in chromatin state, elaborating the effect of the circadian coincidence timer. Hence, circadian clock-pituitary epigenetic pathway interactions form the basis of the mammalian coincidence timer mechanism. Our results constitute a blueprint for circadian-based seasonal timekeeping in vertebrates.

Date: 2020
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DOI: 10.1038/s41467-020-18061-z

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