IDEAS home Printed from https://ideas.repec.org/a/nat/natcom/v6y2015i1d10.1038_ncomms10126.html
   My bibliography  Save this article

Engulfment pathways promote programmed cell death by enhancing the unequal segregation of apoptotic potential

Author

Listed:
  • Sayantan Chakraborty

    (Ludwig-Maximilians-University, Munich, Center for Integrated Protein Science Munich—CIPSM, LMU Biocenter, Planegg-Martinsried)

  • Eric J. Lambie

    (Ludwig-Maximilians-University, Munich, Center for Integrated Protein Science Munich—CIPSM, LMU Biocenter, Planegg-Martinsried)

  • Samik Bindu

    (Ludwig-Maximilians-University, Munich, Center for Integrated Protein Science Munich—CIPSM, LMU Biocenter, Planegg-Martinsried
    5841 S. Maryland Ave., Chicago, Illinosis)

  • Tamara Mikeladze-Dvali

    (Ludwig-Maximilians-University, Munich, Center for Integrated Protein Science Munich—CIPSM, LMU Biocenter, Planegg-Martinsried)

  • Barbara Conradt

    (Ludwig-Maximilians-University, Munich, Center for Integrated Protein Science Munich—CIPSM, LMU Biocenter, Planegg-Martinsried)

Abstract

Components of the conserved engulfment pathways promote programmed cell death in Caenorhabditis elegans (C. elegans) through an unknown mechanism. Here we report that the phagocytic receptor CED-1 mEGF10 is required for the formation of a dorsal–ventral gradient of CED-3 caspase activity within the mother of a cell programmed to die and an increase in the level of CED-3 protein within its dying daughter. Furthermore, CED-1 becomes enriched on plasma membrane regions of neighbouring cells that appose the dorsal side of the mother, which later forms the dying daughter. Therefore, we propose that components of the engulfment pathways promote programmed cell death by enhancing the polar localization of apoptotic factors in mothers of cells programmed to die and the unequal segregation of apoptotic potential into dying and surviving daughters. Our findings reveal a novel function of the engulfment pathways and provide a better understanding of how apoptosis is initiated during C. elegans development.

Suggested Citation

  • Sayantan Chakraborty & Eric J. Lambie & Samik Bindu & Tamara Mikeladze-Dvali & Barbara Conradt, 2015. "Engulfment pathways promote programmed cell death by enhancing the unequal segregation of apoptotic potential," Nature Communications, Nature, vol. 6(1), pages 1-9, December.
  • Handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms10126
    DOI: 10.1038/ncomms10126
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/ncomms10126
    File Function: Abstract
    Download Restriction: no

    File URL: https://libkey.io/10.1038/ncomms10126?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
    ---><---

    Citations

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


    Cited by:

    1. Nadin Memar & Ryan Sherrard & Aditya Sethi & Carla Lloret Fernandez & Henning Schmidt & Eric J. Lambie & Richard J. Poole & Ralf Schnabel & Barbara Conradt, 2024. "The replicative helicase CMG is required for the divergence of cell fates during asymmetric cell division in vivo," Nature Communications, Nature, vol. 15(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:natcom:v:6:y:2015:i:1:d:10.1038_ncomms10126. 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.