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Developmental Cell
Article
License: Elsevier Non-Commercial
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Developmental Cell
Article . 2006
License: Elsevier Non-Commercial
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Developmental Cell
Article . 2006 . Peer-reviewed
License: Elsevier Non-Commercial
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Rap-GEF Signaling Controls Stem Cell Anchoring to Their Niche through Regulating DE-Cadherin-Mediated Cell Adhesion in the Drosophila Testis

Authors: Wang, Hong; Singh, Shree Ram; Zheng, Zhiyu; Oh, Su-Wan; Chen, Xiu; Edwards, Kevin; Hou, Steven X.;

Rap-GEF Signaling Controls Stem Cell Anchoring to Their Niche through Regulating DE-Cadherin-Mediated Cell Adhesion in the Drosophila Testis

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 Drosophila testes, 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 signaling/E-cadherin pathway may represent one mechanism that regulates polarized niche formation and stem cell anchoring.

Keywords

Male, Embryo, Nonmammalian, Cell Adhesion Molecules, Neuronal, Green Fluorescent Proteins, Models, Biological, Animals, Genetically Modified, DEAD-box RNA Helicases, Cell Adhesion, Animals, Drosophila Proteins, Guanine Nucleotide Exchange Factors, Cloning, Molecular, In Situ Hybridization, Cadherins, STEMCELL, Immunohistochemistry, ErbB Receptors, STAT Transcription Factors, SIGNALING, Mutation, CELLBIO, Drosophila, RNA Helicases, Developmental Biology

  • BIP!
    Impact byBIP!
    citations
    This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
    102
    popularity
    This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
    Top 10%
    influence
    This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
    Top 10%
    impulse
    This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
    Top 10%
Powered by OpenAIRE graph
citations
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
102
Top 10%
Top 10%
Top 10%
hybrid