title: Disrupted light-dark cycle abolishes circadian expression of peripheral clock genes without inducing behavioral arrhythmicity in mice.
abstract: The environmental light-dark (LD) cycle entrains the central circadian clock located in the suprachiasmatic nucleus (SCN) of mammals. The present study examined the effects of disrupted LD cycles on peripheral clocks in mice housed under a normal 12 h light-12 h dark cycle (LD 12:12) or an ultradian LD 3:3 cycle. Drinking behavior seemed to be free-running with a long period (26.03 h) under ultradian LD 3:3 cycles, in addition to light-induced direct suppression (masking effect). Core body temperature completely lost robust circadian rhythm and acquired a 6-h rhythm with a low amplitude under LD 3:3. Robust circadian expression of Per1, Per2, Clock and Bmal1 mRNAs was similarly flattened to intermediate levels in the liver, heart and white adipose tissue under LD 3:3. Robust circadian expression of Rev-erbα mRNA was completely damped in these tissues. Circadian expression of Dbp, a clock-controlled gene, was also disrupted in these tissues from mice housed under LD 3:3. The aberrant LD cycle seemed to induce the loss of circadian gene expression at the level of transcription, because rhythmic pre-mRNA expression of these genes was also abolished under LD 3:3. In addition to the direct effect of the aberrant LD cycle, abolished systemic time cues such as those of plasma corticosterone and body temperature might be involved in the disrupted expression of these circadian genes under LD 3:3. Our findings suggest that disrupted environmental LD cycles abolish the normal oscillation of peripheral clocks and induce internal desynchrony in mammals.
authors: Biological Clock Research Group, Biomedical Research Institute, National Institute of Advanced Industrial Science and Technology (AIST), Tsukuba, Ibaraki 305-8566, Japan; Department of Applied Biological Science, Graduate School of Science and Technology, Tokyo University of Science, Noda, Chiba 278-8510, Japan; Department of Medical Genome Sciences, Graduate School of Frontier Sciences, University of Tokyo, Kashiwa, Chiba 277-0882, Japan. Electronic address: k-ooishi@aist.go.jp.
authors: Katsutaka
authors: K
authors: Oishi
authors: Biological Clock Research Group, Biomedical Research Institute, National Institute of Advanced Industrial Science and Technology (AIST), Tsukuba, Ibaraki 305-8566, Japan.
authors: Sayaka
authors: S
authors: Higo-Yamamoto
authors: Biological Clock Research Group, Biomedical Research Institute, National Institute of Advanced Industrial Science and Technology (AIST), Tsukuba, Ibaraki 305-8566, Japan.
authors: Saori
authors: S
authors: Yamamoto
authors: Biological Clock Research Group, Biomedical Research Institute, National Institute of Advanced Industrial Science and Technology (AIST), Tsukuba, Ibaraki 305-8566, Japan; Department of Applied Biological Science, Graduate School of Science and Technology, Tokyo University of Science, Noda, Chiba 278-8510, Japan.
authors: Yuki
authors: Y
authors: Yasumoto
mesh_terms: D000818:Animals; D001522:Behavior, Animal / Q000502:physiology*; D001683:Biological Clocks / Q000502:physiology; D001831:Body Temperature / Q000502:physiology*; D057906:Circadian Clocks / Q000502:physiology*; D056925:Circadian Rhythm Signaling Peptides and Proteins / Q000378:metabolism*; D015536:Down-Regulation / Q000502:physiology; D051379:Mice; D008813:Mice, Inbred ICR; D009043:Motor Activity / Q000502:physiology*; D009928:Organ Specificity; D017440:Photoperiod; D014018:Tissue Distribution
chemical_list: D056925:Circadian Rhythm Signaling Peptides and Proteins
keywords: Body temperature; Circadian rhythm; Clock gene; Internal desynchrony; Peripheral clock; Ultradian light–dark cycle