FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
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Citation
Sung, H.H., Li, H., Huang, Y.C., Ai, C.L., Hsieh, M.Y., Jan, H.M., Peng, Y.J., Lin, H.Y., Yeh, C.H., Lin, S.Y., Yeh, C.Y., Cheng, Y.J., Khoo, K.H., Lin, C.H., Chien, C.T. (2024). Galectins induced from hemocytes bridge phosphatidylserine and N-glycosylated Drpr/CED-1 receptor during dendrite pruning.  Nat. Commun. 15(1): 7402.
FlyBase ID
FBrf0260325
Publication Type
Research paper
Abstract
During neuronal pruning, phagocytes engulf shed cellular debris to avoid inflammation and maintain tissue homeostasis. How phagocytic receptors recognize degenerating neurites had been unclear. Here, we identify two glucosyltransferases Alg8 and Alg10 of the N-glycosylation pathway required for dendrite fragmentation and clearance through genetic screen. The scavenger receptor Draper (Drpr) is N-glycosylated with complex- or hybrid-type N-glycans that interact specifically with galectins. We also identify the galectins Crouching tiger (Ctg) and Hidden dragon (Hdg) that interact with N-glycosylated Drpr and function in dendrite pruning via the Drpr pathway. Ctg and Hdg are required in hemocytes for expression and function, and are induced during dendrite injury to localize to injured dendrites through specific interaction with exposed phosphatidylserine (PS) on the surface membrane of injured dendrites. Thus, the galectins Ctg and Hdg bridge the interaction between PS and N-glycosylated Drpr, leading to the activation of phagocytosis.
PubMed ID
PubMed Central ID
PMC11349873 (PMC) (EuropePMC)
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Assignment of cell line based on information provided by the author in the Fast Track Your Paper tool.
FlyBase Curators, 2020-, Assignment of cell line based on information provided by the author in the Fast Track Your Paper tool. [FBrf0247694]

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Secondary IDs
    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    Nat. Commun.
    Title
    Nature communications
    ISBN/ISSN
    2041-1723
    Data From Reference