FB2026_03 , released September 17, 2026
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Citation
Yatsenko, A.S., Shcherbata, H.R. (2014). Drosophila miR-9a Targets the ECM Receptor Dystroglycan to Canalize Myotendinous Junction Formation.  Dev. Cell 28(3): 335--348.
FlyBase ID
FBrf0224114
Publication Type
Research paper
Abstract
Establishment of intercellular interactions between various cell types of different origin is vital for organism development and tissue maintenance. Therefore, precise timing, expression pattern, and amounts of extracellular matrix (ECM) proteins must be tightly regulated. Particularly, the ECM is important for the development and function of myotendinous junctions (MTJs). We find that precise levels of the ECM receptor Dystroglycan (Dg) are required for MTJ formation in Drosophila and that Dg levels in this process are controlled by miR-9a. In the embryo, Dg is enriched at the termini of the growing muscles facing the tendon matrix and absent from miR-9a-expressing tendons. This gradient of Dg expression is crucial for proper muscle-tendon attachments and is adjusted by miR-9a. In addition to Dg, miR-9a regulates the expression of several other critical muscle genes, and we therefore propose that during embryogenesis, miR-9a specifically controls the expression of mesodermal genes to canalize MTJ morphogenesis.
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Obtained with permission from Cell Press.
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    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    Dev. Cell
    Title
    Developmental Cell
    Publication Year
    2001-
    ISBN/ISSN
    1534-5807 1878-1551
    Data From Reference
    Genes (17)
    Human Disease Models (1)
    Physical Interactions (13)
    Cell Lines (1)