IDEAS home Printed from https://ideas.repec.org/a/nat/natcom/v7y2016i1d10.1038_ncomms10473.html
   My bibliography  Save this article

The novel tumour suppressor Madm regulates stem cell competition in the Drosophila testis

Author

Listed:
  • Shree Ram Singh

    (The Basic Research Laboratory, National Cancer Institute, National Institutes of Health)

  • Ying Liu

    (The Basic Research Laboratory, National Cancer Institute, National Institutes of Health)

  • Jiangsha Zhao

    (The Basic Research Laboratory, National Cancer Institute, National Institutes of Health)

  • Xiankun Zeng

    (The Basic Research Laboratory, National Cancer Institute, National Institutes of Health)

  • Steven X. Hou

    (The Basic Research Laboratory, National Cancer Institute, National Institutes of Health)

Abstract

Stem cell competition has emerged as a mechanism for selecting fit stem cells/progenitors and controlling tumourigenesis. However, little is known about the underlying molecular mechanism. Here we identify Mlf1-adaptor molecule (Madm), a novel tumour suppressor that regulates the competition between germline stem cells (GSCs) and somatic cyst stem cells (CySCs) for niche occupancy. Madm knockdown results in overexpression of the EGF receptor ligand vein (vn), which further activates EGF receptor signalling and integrin expression non-cell autonomously in CySCs to promote their overproliferation and ability to outcompete GSCs for niche occupancy. Conversely, expressing a constitutively activated form of the Drosophila JAK kinase (hopTum−l) promotes Madm nuclear translocation, and suppresses vn and integrin expression in CySCs that allows GSCs to outcompete CySCs for niche occupancy and promotes GSC tumour formation. Tumour suppressor-mediated stem cell competition presented here could be a mechanism of tumour initiation in mammals.

Suggested Citation

  • Shree Ram Singh & Ying Liu & Jiangsha Zhao & Xiankun Zeng & Steven X. Hou, 2016. "The novel tumour suppressor Madm regulates stem cell competition in the Drosophila testis," Nature Communications, Nature, vol. 7(1), pages 1-12, April.
    • Handle: RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms10473
    DOI: 10.1038/ncomms10473
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/ncomms10473
    File Function: Abstract
    Download Restriction: no
    File URL: https://libkey.io/10.1038/ncomms10473?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
    ---><---

    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:7:y:2016:i:1:d:10.1038_ncomms10473. 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.