FB2026_03 , released September 17, 2026
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Citation
Ho, K.Y.L., An, K., Carr, R.L., Dvoskin, A.D., Ou, A.Y.J., Vogl, W., Tanentzapf, G. (2023). Maintenance of hematopoietic stem cell niche homeostasis requires gap junction-mediated calcium signaling.  Proc. Natl. Acad. Sci. U.S.A. 120(45): e2303018120.
FlyBase ID
FBrf0257898
Publication Type
Research paper
Abstract
Regulation of stem cells requires coordination of the cells that make up the stem cell niche. Here, we describe a mechanism that allows communication between niche cells to coordinate their activity and shape the signaling environment surrounding resident stem cells. Using the Drosophila hematopoietic organ, the lymph gland, we show that cells of the hematopoietic niche, the posterior signaling center (PSC), communicate using gap junctions (GJs) and form a signaling network. This network allows PSC cells to exchange Ca[2+] signals repetitively which regulate the hematopoietic niche. Disruption of Ca[2+] signaling in the PSC or the GJ-mediated network connecting niche cells causes dysregulation of the PSC and blood progenitor differentiation. Analysis of PSC-derived cell signaling shows that the Hedgehog pathway acts downstream of GJ-mediated Ca[2+] signaling to modulate the niche microenvironment. These data show that GJ-mediated communication between hematopoietic niche cells maintains their homeostasis and consequently controls blood progenitor behavior.
PubMed ID
PubMed Central ID
PMC10636368 (PMC) (EuropePMC)
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Secondary IDs
    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    Proc. Natl. Acad. Sci. U.S.A.
    Title
    Proceedings of the National Academy of Sciences of the United States of America
    Publication Year
    1915-
    ISBN/ISSN
    0027-8424
    Data From Reference
    Genes (19)