FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
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Citation
Wang, Y., Zhang, R., Huang, S., Valverde, P.T.T., Lobb-Rabe, M., Ashley, J., Venkatasubramanian, L., Carrillo, R.A. (2023). Glial Draper signaling triggers cross-neuron plasticity in bystander neurons after neuronal cell death in Drosophila.  Nat. Commun. 14(1): 4452.
FlyBase ID
FBrf0257083
Publication Type
Research paper
Abstract
Neuronal cell death and subsequent brain dysfunction are hallmarks of aging and neurodegeneration, but how the nearby healthy neurons (bystanders) respond to the death of their neighbors is not fully understood. In the Drosophila larval neuromuscular system, bystander motor neurons can structurally and functionally compensate for the loss of their neighbors by increasing their terminal bouton number and activity. We term this compensation as cross-neuron plasticity, and in this study, we demonstrate that the Drosophila engulfment receptor, Draper, and the associated kinase, Shark, are required for cross-neuron plasticity. Overexpression of the Draper-I isoform boosts cross-neuron plasticity, implying that the strength of plasticity correlates with Draper signaling. In addition, we find that functional cross-neuron plasticity can be induced at different developmental stages. Our work uncovers a role for Draper signaling in cross-neuron plasticity and provides insights into how healthy bystander neurons respond to the loss of their neighboring neurons.
PubMed ID
PubMed Central ID
PMC10366216 (PMC) (EuropePMC)
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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