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Ying Zhang, Nan Meng, Haili Bao, Yufei Jiang, Ningjie Yang, Kejia Wu, Jinxiang Wu, Haibin Wang, Shuangbo Kong and Yuanzhen Zhang

altered by ovarian hormones ( Johnson et al. 2002 , Nakamura et al. 2005 , 2008 , 2010 , He et al. 2007 , Hirata et al. 2009 ). PER2 deficiency leads to flattened diurnal oscillation of all the core clock genes and to disorganized decidual

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GA Lincoln, H Andersson and A Loudon

Melatonin-based photoperiod time-measurement and circannual rhythm generation are long-term time-keeping systems used to regulate seasonal cycles in physiology and behaviour in a wide range of mammals including man. We summarise recent evidence that temporal, melatonin-controlled expression of clock genes in specific calendar cells may provide a molecular mechanism for long-term timing. The agranular secretory cells of the pars tuberalis (PT) of the pituitary gland provide a model cell-type because they express a high density of melatonin (mt1) receptors and are implicated in photoperiod/circannual regulation of prolactin secretion and the associated seasonal biological responses. Studies of seasonal breeding hamsters and sheep indicate that circadian clock gene expression in the PT is modulated by photoperiod via the melatonin signal. In the Syrian and Siberian hamster PT, the high amplitude Per1 rhythm associated with dawn is suppressed under short photoperiods, an effect that is mimicked by melatonin treatment. More extensive studies in sheep show that many clock genes (e.g. Bmal1, Clock, Per1, Per2, Cry1 and Cry2) are expressed in the PT, and their expression oscillates through the 24-h light/darkness cycle in a temporal sequence distinct from that in the hypothalamic suprachiasmatic nucleus (central circadian pacemaker). Activation of Per1 occurs in the early light phase (dawn), while activation of Cry1 occurs in the dark phase (dusk), thus photoperiod-induced changes in the relative phase of Per and Cry gene expression acting through PER/CRY protein/protein interaction provide a potential mechanism for decoding the melatonin signal and generating a long-term photoperiodic response. The current challenge is to identify other calendar cells in the central nervous system regulating long-term cycles in reproduction, body weight and other seasonal characteristics and to establish whether clock genes provide a conserved molecular mechanism for long-term timekeeping.

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Jonathan D Johnston and Debra J Skene

). Altered sensitisation of PT cells by physiologically encountered melatonin signals may therefore contribute to photoperiodic timing mechanisms. Identification of clock gene expression in the PT ( Sun et al . 1997 ) invited speculation that there may be

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Michaela D Wharfe, Peter J Mark, Caitlin S Wyrwoll, Jeremy T Smith, Cassandra Yap, Michael W Clarke and Brendan J Waddell

part by the rhythmic expression of clock genes in the suprachiasmatic nucleus (SCN) ( Nader et al . 2010 ). These clock genes ( Bmal1/Arntl , Clock , Per1 , Per2 , Cry1 and Cry2 ) form a molecular network of transcriptional–translational loops to

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J Fahrenkrug, B Georg, J Hannibal and H L Jørgensen

cells, the molecular machinery is composed of the same clock genes and their protein products connected by autoregulatory feedback loops. The major loop comprises the PAS domain helix-loop-helix transcriptional activators BMAL1 and CLOCK forming

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Cassandra C Yap, Michaela D Wharfe, Peter J Mark, Brendan J Waddell and Jeremy T Smith

, the SCN exerts tight circadian control over many biological processes through endogenous rhythms generated by positive and negative feedback gene transcription and translation loops of clock genes, including Clock , Bmal1 , Per1-3 , Cry 1-2 , and

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Esther Isorna, Nuria de Pedro, Ana I Valenciano, Ángel L Alonso-Gómez and María J Delgado

located in numerous (if not all) tissues ( Fig. 1 ). The molecular functioning of this set of oscillators is similar in peripheral and central clocks and is based on translational–transcriptional feedback loops of a set of genes called clock genes, whose

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Pei-Jian He, Masami Hirata, Nobuhiko Yamauchi and Masa-aki Hattori

expression, and thus synchronize or reset the circadian rhythms in cultured cells. For instance, glucocorticoids could efficiently activate Per1 expression and synchronizes circadian oscillations of clock genes in cultured cells, and could also phase shift

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Pei-Jian He, Masami Hirata, Nobuhiko Yamauchi, Seiichi Hashimoto and Masa-aki Hattori

secretion and metabolisms like gluconeogenesis and lipogenesis ( Lemos et al. 2006 , Wijnen & Young 2006 ). Interestingly, cultured cell lines could also exhibit several cycles of oscillations of the clock genes when treated with dexamethasone (DXM), a

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Shanqi Fu, Miho Kuwahara, Yoko Uchida, Sei Kondo, Daichi Hayashi, Yuji Shimomura, Asami Takagaki, Takashi Nishida, Yusuke Maruyama, Mika Ikegame, Atsuhiko Hattori, Satoshi Kubota and Takako Hattori

rhythm that persisted for several months in both articular and growth plate cartilage ( Okubo et al. 2013 ). Recently, several studies have demonstrated the rhythmic expression of clock genes in cartilage, indicating that, similar to the central SCN