Circadian Clock Gene Per2 Is Not Necessary for the Photoperiodic Response in Mice

Abstract

In mammals, light information received by the eyes is transmitted to the pineal gland via the circadian pacemaker, i.e., the suprachiasmatic nucleus (SCN). Melatonin secreted by the pineal gland at night decodes night length and regulates seasonal physiology and behavior. Melatonin regulates the expression of the β-subunit of thyroid-stimulating hormone (TSH; Tshb) in the pars tuberalis (PT) of the pituitary gland. Long day-induced PT TSH acts on ependymal cells in the mediobasal hypothalamus to induce the expression of type 2 deiodinase (Dio2) and reduce type 3 deiodinase (Dio3) that are thyroid hormone-activating and hormone-inactivating enzymes, respectively. The long day-activated thyroid hormone T3 regulates seasonal gonadotropin-releasing hormone secretion. It is well established that the circadian clock is involved in the regulation of photoperiodism. However, the involvement of the circadian clock gene in photoperiodism regulation remains unclear. Although mice are generally considered non-seasonal animals, it was recently demonstrated that mice are a good model for the study of photoperiodism. In the present study, therefore, we examined the effect of changing day length in Per2 deletion mutant mice that show shorter wheel-running rhythms under constant darkness followed by arhythmicity. Although the amplitude of clock gene (Per1, Cry1) expression was greatly attenuated in the SCN, the expression profile of arylalkylamine N-acetyltransferase, a rate-limiting melatonin synthesis enzyme, was unaffected in the pineal gland, and robust photoperiodic responses of the Tshb, Dio2, and Dio3 genes were observed. These results suggested that the Per2 clock gene is not necessary for the photoperiodic response in mice.

Transcriptional profiling of SHR/NCrl prefrontal cortex shows hyperactivity‐associated genes responsive to amphetamine challenge

“…and high mortality (Yvert et al 2000;Noma et al 2012). Genes in this family encode components of the circadian rhythms of locomotor activity, metabolism and behavior (Ikegami et al 2013;Zhu et al 2014). However, no study has described an association between Atxn7 and ADHD and this study, to the best of our knowledge, is the first to describe such association.…”

Cry1 deficiency leads to testicular dysfunction and altered expression of genes involved in cell communication, chromatin reorganization, spermatogenesis, and immune response in mouse testis

“…A previous study reported that Per2 expression in the kidney, small intestine, and skin was upregulated at an earlier time point in Cry1 KO and later in Cry2 KO mice as compared to their WT counterparts (Destici et al, ). Although the rhythmic expression of Cry1 in the SCN was unaltered in Per2 mutant mice, the level was greatly reduced (Ikegami, Iigo, & Yoshimura, ). This suggests an interaction between Cry1 and Per2 that is tissue specific.…”

Effect of summer daylight exposure and genetic background on growth in growth hormone-deficient children

“…34 The link between day length and melatonin secretion resides in the eye, a light-sensitive organ whose function is to maintain circadian and seasonal rhythms, 35 as facilitated by retinal communication via neural tracts with the pineal gland. 35, 36 A circadian clock has been found to be primarily mediated by melanopsin-containing retinal ganglion cells, 36, 37, 38 which are intrinsically blue-light sensitive. 39 A number of studies have also provided support for a link between seasonal changes in daylight and physiological alterations, including human growth, 40, 41 with the existence of a seasonal variability in growth patterns in normal children.…”