IDEAS home Printed from https://ideas.repec.org/a/nat/nature/v387y1997i6636d10.1038_43191.html
   My bibliography  Save this article

Fringe modulates Notch–ligand interactions

Author

Listed:
  • Vladislav M. Panin
  • Venizelos Papayannopoulos
  • Richa Wilson
  • Kenneth D. Irvine

    (Rutgers, The State University)

Abstract

The Notch family of transmembrane receptor proteins mediate developmental cell-fate decisions1, and mutations in mammalian Notch genes have been implicated in leukaemia, breast cancer, stroke and dementia2,3,4. During wing development in Drosophila, the Notch receptor is activated along the border between dorsal and ventral cells5,6,7, leading to the specification of specialized cells that express Wingless (Wg) and organize wing growth and patterning6,8,9. Three genes, fringe (fng), Serrate (Ser) and Delta (Dl), are involved in the cellular interactions leading to Notch activation7,9,10,11,12,13,14,15. Ser and Dl encode transmembrane ligands for Notch16,17, whereas fng encodes a pioneer protein10. We have investigated the relationship between these genes by a combination of expression and coexpression studies in the Drosophila wing. We found that Ser and Dl maintain each other's expression by a positive feedback loop. fng is expressed specifically by dorsal cells and functions to position and restrict this feedback loop to the developing dorsal–ventral boundary. This is achieved by fng through a cell-autonomous mechanism that inhibits a cell's ability to respond to Serrate protein and potentiates its ability to respond to Delta protein.

Suggested Citation

  • Vladislav M. Panin & Venizelos Papayannopoulos & Richa Wilson & Kenneth D. Irvine, 1997. "Fringe modulates Notch–ligand interactions," Nature, Nature, vol. 387(6636), pages 908-912, June.
  • Handle: RePEc:nat:nature:v:387:y:1997:i:6636:d:10.1038_43191
    DOI: 10.1038/43191
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/43191
    File Function: Abstract
    Download Restriction: Access to the full text of the articles in this series is restricted.

    File URL: https://libkey.io/10.1038/43191?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.

    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:387:y:1997:i:6636:d:10.1038_43191. 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.