Rap-GEF Signaling Controls Stem Cell Anchoring to Their Niche through Regulating DE-Cadherin-Mediated Cell Adhesion in the Drosophila Testis
pmid: 16399083
Rap-GEF Signaling Controls Stem Cell Anchoring to Their Niche through Regulating DE-Cadherin-Mediated Cell Adhesion in the Drosophila Testis
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.
- National Institutes of Health United States
- National Institute of Health Pakistan
- Illinois State University United States
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
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
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