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. 2020 Aug 27;11:4291. doi: 10.1038/s41467-020-18061-z

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 6 — The photoperiod sculpts the duration of the melatonin signal, long duration on short photoperiods (SP, winter) and short duration on long photoperiods (LP, summer). In the pars tuberalis approximately 12 hours after the onset of darkness there is a photosensitive phase. When this phase coincides with light BMAL2 is expressed. When this phase is coincident with darkness DEC1 is expressed. This forms a photoperiodic flip-flop switch between two stable states. The role of BMAL2, CLOCK and BMAL1 is to co-activate EYA3 and subsequently seasonal physiological changes. DEC1 suppresses the E-box based activation of EYA3. Also occurring in the dark phase of SP a number of repressors are expressed which target appear to target LP induced genes potentially inhibiting the expression of summer physiology. Aside from this acute photoperiodic flip-flop switch there is a progressive photoperiod dependent epigenetic regulation over a number of weeks augmenting the coincidence based timer drive on summer physiology.