CLOCK:BMAL-Independent Circadian Oscillation of Zebrafish Cryptochrome1a Gene

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  • Miyamura Norio
    Department of Developmental and Regenerative Biology, Tokyo Medical and Dental University
  • Hirayama Jun
    Medical Top Track Program, Medical Research Institute, Tokyo Medical and Dental University
  • Sawanobori Kenji
    Department of Developmental and Regenerative Biology, Tokyo Medical and Dental University Department of Physiological Chemistry, Graduate School of Pharmaceutical Sciences, University of Tokyo
  • Tamaru Teruya
    Department of Physiology, Toho University School of Medicine
  • Asaoka Yoichi
    Department of Developmental and Regenerative Biology, Tokyo Medical and Dental University
  • Honda Reiko
    Medical Top Track Program, Medical Research Institute, Tokyo Medical and Dental University
  • Yamamoto Takuro
    Life Science Laboratory, Advanced Materials Laboratories, Sony Corporation
  • Uno Hatsume
    Life Science Laboratory, Advanced Materials Laboratories, Sony Corporation
  • Takamatsu Ken
    Department of Physiology, Toho University School of Medicine
  • Nishina Hiroshi
    Department of Developmental and Regenerative Biology, Tokyo Medical and Dental University

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Abstract

In the vertebrate circadian feedback loop, CLOCK:BMAL heterodimers induce the expression of Cry genes. The CRY proteins in turn inhibit CLOCK:BMAL-mediated transcription closing the negative feedback loop. Four CRYs, which all inhibit CLOCK:BMAL-mediated transcription, exist in zebrafish. Although these zebrafish Crys (zCry1a, 1b, 2a, and 2b) show a circadian pattern of expression, previous studies have indicated that the circadian oscillation of zCry1a could be CLOCK:BMAL-independent. Here we show that abrogation of CLOCK:BMAL-dependent transcription in zebrafish cells by the dominant negative zCLOCK3-DeltaC does not affect the circadian oscillation of zCry1a. Moreover, we provide several lines of evidence indicating that the extracellular signal-regulated kinase (ERK) signaling cascade modulates the circadian expression of zCry1a gene in constant darkness. Taken together, our data strongly support the notion that circadian oscillation of zCry1a is CLOCK:BMAL-independent and further indicate that mechanisms involving non-canonical clock genes could contribute to the circadian expression of zCry1a gene in a cell autonomous manner.

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