Skip NavigationSkip to Content
Return Return to Search Results

Rap-GEF signaling controls stem cell anchoring to their niche through regulating DE-cadherin-mediated cell adhesion in the Drosophila testis

  1. Author:
    Wang, H.
    Singh, S. R.
    Zheng, Z. Y.
    Oh, S. W.
    Chen, X.
    Edwards, K.
    Hou, S. X.

  2. Author Address

    NCI, Immunobiol Lab, NIH, Frederick, MD 21702 USA. Illinois State Univ, Dept Biol Sci, Normal, IL 61790 USA Hou, SX, NCI, Immunobiol Lab, NIH, Frederick, MD 21702 USA
    1. Year: 2006
    2. Date: JAN
  2. Journal: Developmental Cell
    1. 10
    2. 1
    3. Pages: 117-126
  4. Type of Article: Article
  1. Abstract:

    Stem cells will undergo self-renewal to produce new stem cells if they are maintained in their niches. The regulatory mechanisms that recruit and maintain stem cells in their niches are not well understood. In Drosophilatestes, a group of 12 nondividing somatic cells, called the hub, identifies the stem cell niche by producing the growth factor Unpaired (Upd). Here, we show that Rap-GEF/Rap signaling controls stem cell anchoring to the niche through regulating DE-cadherin-mediated cell adhesion. Loss of function of a Drosophila Rap-GEF (Gef26) results in loss of both germline and somatic stem cells. The Gef26 mutation specifically impairs adherens junctions at the hub-stem cell interface, which results in the stem cells "drifting away" from the niche and losing stem cell identity. Thus, the Rap signal ing/E-cadherin pathway may represent one mechanism that regulates polarized niche formation and stem cell anchoring

    See More

  1. Keywords:

External Sources

  1. View Full Text
  2. DOI: 10.1016/j.devcel.2005.11.004
  3. View record in Web of Science®
  4. WOS: 000234935500015

Library Notes

  1. No notes added.
NCI at Frederick

You are leaving a government website.

This external link provides additional information that is consistent with the intended purpose of this site. The government cannot attest to the accuracy of a non-federal site.

Linking to a non-federal site does not constitute an endorsement by this institution or any of its employees of the sponsors or the information and products presented on the site. You will be subject to the destination site's privacy policy when you follow the link.

ContinueCancel