IDEAS home Printed from https://ideas.repec.org/a/nat/nature/v398y1999i6728d10.1038_19323.html
   My bibliography  Save this article

Mammalian Cry1 and Cry2 are essential for maintenance of circadian rhythms

Author

Listed:
  • Gijsbertus T. J. van der Horst

    (MGC, Erasmus University)

  • Manja Muijtjens

    (MGC, Erasmus University)

  • Kumiko Kobayashi

    (Institute of Development, Aging and Cancer, Tohoku University)

  • Riya Takano

    (Institute of Development, Aging and Cancer, Tohoku University)

  • Shin-ichiro Kanno

    (Institute of Development, Aging and Cancer, Tohoku University)

  • Masashi Takao

    (Institute of Development, Aging and Cancer, Tohoku University)

  • Jan de Wit

    (MGC, Erasmus University)

  • Anton Verkerk

    (MGC, Erasmus University)

  • Andre P. M. Eker

    (MGC, Erasmus University)

  • Dik van Leenen

    (MGC, Erasmus University)

  • Ruud Buijs

    (Netherlands Institute for Brain Research)

  • Dirk Bootsma

    (MGC, Erasmus University)

  • Jan H. J. Hoeijmakers

    (MGC, Erasmus University)

  • Akira Yasui

    (Institute of Development, Aging and Cancer, Tohoku University)

Abstract

Many biochemical, physiological and behavioural processes show circadian rhythms which are generated by an internal time-keeping mechanism referred to as the biological clock. According to rapidly developing models, the core oscillator driving this clockis composed of an autoregulatory transcription–(post) translation-based feedback loop involving a set of ‘clock’ genes1,6. Molecular clocks do not oscillate with an exact 24-hour rhythmicity but are entrained to solar day/night rhythms by light. The mammalian proteins Cry1 and Cry2, which are members of the family of plant blue-light receptors (cryptochromes) and photolyases, have been proposed as candidate light receptors for photoentrainment of the biological clock7,8,9,10. Here we show that mice lacking the Cry1 or Cry2 protein display accelerated and delayed free-running periodicity of locomotor activity, respectively. Strikingly, in the absence of both proteins, an instantaneous and complete loss of free-running rhythmicity is observed. This suggests that, in addition to a possible photoreceptor and antagonistic clock-adjusting function, both proteins are essential for the maintenance of circadian rhythmicity.

Suggested Citation

  • Gijsbertus T. J. van der Horst & Manja Muijtjens & Kumiko Kobayashi & Riya Takano & Shin-ichiro Kanno & Masashi Takao & Jan de Wit & Anton Verkerk & Andre P. M. Eker & Dik van Leenen & Ruud Buijs & Di, 1999. "Mammalian Cry1 and Cry2 are essential for maintenance of circadian rhythms," Nature, Nature, vol. 398(6728), pages 627-630, April.
  • Handle: RePEc:nat:nature:v:398:y:1999:i:6728:d:10.1038_19323
    DOI: 10.1038/19323
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/19323
    File Function: Abstract
    Download Restriction: Access to the full text of the articles in this series is restricted.

    File URL: https://libkey.io/10.1038/19323?utm_source=ideas
    LibKey link: if access is restricted and if your library uses this service, LibKey will redirect you to where you can use your library subscription to access this item
    ---><---

    As the access to this document is restricted, you may want to search for a different version of it.

    Citations

    Citations are extracted by the CitEc Project, subscribe to its RSS feed for this item.
    as


    Cited by:

    1. Yasuko O. Abe & Hikari Yoshitane & Dae Wook Kim & Satoshi Kawakami & Michinori Koebis & Kazuki Nakao & Atsu Aiba & Jae Kyoung Kim & Yoshitaka Fukada, 2022. "Rhythmic transcription of Bmal1 stabilizes the circadian timekeeping system in mammals," Nature Communications, Nature, vol. 13(1), pages 1-12, December.
    2. Yang An & Baoshi Yuan & Pancheng Xie & Yue Gu & Zhiwei Liu & Tao Wang & Zhihao Li & Ying Xu & Yi Liu, 2022. "Decoupling PER phosphorylation, stability and rhythmic expression from circadian clock function by abolishing PER-CK1 interaction," Nature Communications, Nature, vol. 13(1), pages 1-17, December.
    3. Seref Gul & Yasemin Kubra Akyel & Zeynep Melis Gul & Safak Isin & Onur Ozcan & Tuba Korkmaz & Saba Selvi & Ibrahim Danis & Ozgecan Savlug Ipek & Fatih Aygenli & Ali Cihan Taskin & Büşra Aytül Akarlar , 2022. "Discovery of a small molecule that selectively destabilizes Cryptochrome 1 and enhances life span in p53 knockout mice," Nature Communications, Nature, vol. 13(1), pages 1-17, December.

    More about this item

    Statistics

    Access and download statistics

    Corrections

    All material on this site has been provided by the respective publishers and authors. You can help correct errors and omissions. When requesting a correction, please mention this item's handle: RePEc:nat:nature:v:398:y:1999:i:6728:d:10.1038_19323. See general information about how to correct material in RePEc.

    If you have authored this item and are not yet registered with RePEc, we encourage you to do it here. This allows to link your profile to this item. It also allows you to accept potential citations to this item that we are uncertain about.

    We have no bibliographic references for this item. You can help adding them by using this form .

    If you know of missing items citing this one, you can help us creating those links by adding the relevant references in the same way as above, for each refering item. If you are a registered author of this item, you may also want to check the "citations" tab in your RePEc Author Service profile, as there may be some citations waiting for confirmation.

    For technical questions regarding this item, or to correct its authors, title, abstract, bibliographic or download information, contact: Sonal Shukla or Springer Nature Abstracting and Indexing (email available below). General contact details of provider: http://www.nature.com .

    Please note that corrections may take a couple of weeks to filter through the various RePEc services.

    IDEAS is a RePEc service. RePEc uses bibliographic data supplied by the respective publishers.