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Diurnal rhythms in physiological functions contribute to homeostasis in many organisms. Although relationships between molecular biology and diurnal rhythms have been well studied in model organisms like higher plants, those in harmful algal bloom species are poorly understood. Here we measured several physiological parameters and the expression patterns of photosynthesis-related and antioxidant-enzyme genes in the Chattonella marina complex to understand the biological meaning of diurnal rhythm. Under a light–dark cycle, Fv/Fm and expression of psbA, psbD, and 2-Cys prx showed significant increases in the light and decreases during the dark. These rhythms remained even under continuous dark conditions. DCMU suppressed the induction of psbA, psbD, and 2-Cys prx expression under both light regimes. Oxidative stress levels and H2O2 scavenging activities were relatively stable, and there was no significant correlation between H2O2 scavenging activities and antioxidant-enzyme gene expression. These results indicate that the Chattonella marina complex has developed mechanisms for efficient photosynthetic energy production in the light. Our results showed that this species has a diurnal rhythm and a biological clock. These phenomena are thought to contribute to the efficiency of physiological activities centered on photosynthesis and cell growth related to the diurnal vertical movement of this species. [ABSTRACT FROM AUTHOR]

Molecular mechanisms regulating animal seasonal breeding in response to changing photoperiod are not well understood. Rapid induction of gene expression of thyroid-hormone-activating enzyme (type 2 deiodinase, DIO2) in the mediobasal [...]

The molecular basis of seasonal or nonseasonal breeding remains unknown. Although laboratory rats are generally regarded as photoperiod-insensitive species, the testicular weight of the Fischer 344 (F344) strain responds to photoperiod. Recently, it was clarified that photoperiodic regulation of type 2 iodothyronine deiodinase (Dio2) in the mediobasal hypothalamus (MBH) is critical in photoperiodic gonadal regulation. Strain-dependent differences in photoperiod sensitivity may now provide the opportunity to address the regulatory mechanism of seasonality by studying Dio2 expression. Therefore, in the present study, we examined the effect of photoperiod on Dio2 expression in photoperiod-sensitive F344 and photoperiod-insensitive Wistar rats. A statistically significant difference was observed between short and long days in terms of testicular weight and Dio2 expression in the F344 strain, while no difference was observed in the Wistar strain. These results suggest that differential responses of the Dio2 gene to photoperiod may determine the strain-dependent differences in photoperiod sensitivity in laboratory rats. mediobasal hypothalamus; testicular weight; photoperiodism

Photorefractoriness is the insensitivity of gonadal development to the stimulatory effects of long photoperiods in birds and to the inhibitory effects of short photoperiods in small mammals. Its molecular mechanism remains unknown. Recently, it has been shown that reciprocal expression of thyroid hormone-activating enzyme [type 2 deiodinase (Dio2)] and -inactivating enzyme [type 3 deiodinase (Dio3)] genes in the mediobasal hypothalamus is critical for photoperiodically induced gonadal growth. Since thyroid hormones are required not only for photoinduction, but also for the induction of photorefractoriness, we examined the expression of these genes in relation to photorefractoriness in birds and mammals. Transfer of birds to long photoperiods induced strong expression of Dio2. This was maintained in tree sparrow when they later became photorefractory, but decreased somewhat in quail. In hamsters, transfer to long photoperiods also induced strong expression of Dio2. High values were not maintained under long photoperiods, and, indeed, expression decreased at the same rate as in animals transferred to short photoperiods. There was no renewed expression of Dio2 associated with testicular growth as animals became refractory to short photoperiods. Expression of Dio3 was high under short photoperiods and low under long photoperiods in all the animals examined, except for the short photoperiod-refractory hamsters. Our present study revealed complex regulation of deiodinase genes in the photoinduction and photorefractory processes in birds and mammals. These gene changes may be involved in the regulation of photorefractoriness, as well as photoinduction. Eurasian tree sparrow; Japanese quail; Djungarian hamster

Author(s): Takashi Yoshimura (corresponding author) [1]; Shinobu Yasuo [1]; Miwa Watanabe [1]; Masayuki Iigo [3]; Takashi Yamamura [1]; Kanjun Hirunagi [2]; Shizufumi Ebihara [1] Reproduction of many temperate zone birds [...]

Animal studies have shown that irregular light-dark cycles cause circadian desynchronization, while few studies have addressed the effect of regular/irregular stimulation cycles of signaling hormones on the cellular clock in vitro. Here, we examined how cellular clocks respond to regular and irregular stimulation cycles of dexamethasone, using NIH3T3 cells transfected with the Bmal1 promoter-driven luciferase (Bmal1-Luc) reporter gene. Cyclic stimulation with dexamethasone at different time intervals (18–28 h, 3 times regularly) revealed that Bmal1-Luc bioluminescence rhythms can be entrained to 22 and 24 h cycles during the stimulation period, but not to other cycles. The rhythm entrained for 24 h cycles persisted for at least one day after the last stimulation. Irregular dexamethasone treatment (16, 24, and 16 h, sequentially; short-term jet lag protocol) resulted in an overall upregulation and phase shifts of the temporal expression of several clock genes and cell cycle genes, including c-Myc and p53. Regular dexamethasone stimulation three times with 24 h cycles also caused upregulation of Per1 and Per2 expression, but not c-Myc and p53 expression. In conclusion, our study identified the entrainable range of the circadian clock in NIH3T3 cells to the dexamethasone stimulation cycle and demonstrated that irregular dexamethasone treatment could disturb the expression of cell cycle genes. [ABSTRACT FROM AUTHOR]