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Citation
Chohan, Y., Eitzman, E.A., Hawkins, W.D., Klionsky, D.J. (2023). Bruchpiloting synaptic connections: Egfr in autophagy-mediated neuronal circuit development.  Autophagy 19(7): 1899--1900.
FlyBase ID
FBrf0256837
Publication Type
Note
Abstract
Macroautophagy/autophagy is involved in many aspects of human development including the formation of neuronal circuits. A recent study from Dutta et al. found that the recruitment of Egfr (Epidermal growth factor receptor) to synapses suppresses autophagic degradation of presynaptic proteins, a requirement for proper neuronal circuit development. The findings suggest that Egfr inactivation during a distinct critical interval in late development results in increased levels of autophagy in the brain and decreased neuronal circuit development. Furthermore, the presence of brp (bruchpilot) in the synapse is critical for proper neuronal functioning over this same period. Dutta and colleagues found that increased autophagy due to Egfr inactivation results in decreased brp levels and, therefore, reduced neuronal connectivity. Through live cell imaging, it was determined that only the synaptic branches that accumulate both Egfr and brp are stabilized, allowing for the persistence of active zones, further supporting the importance of both Egfr and brp in the brain. While Dutta and colleagues collected these data based on studies conducted on Drosophila brains, the findings provide great insight as to how these different proteins may be implicated in human neurology.
PubMed ID
PubMed Central ID
PMC10283405 (PMC) (EuropePMC)
Related Publication(s)
Research paper

EGFR-dependent suppression of synaptic autophagy is required for neuronal circuit development.
Dutta et al., 2023, Curr. Biol. 33(3): 517--532.e5 [FBrf0255644]

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Secondary IDs
    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    Autophagy
    Title
    Autophagy
    Publication Year
    2005-
    ISBN/ISSN
    1554-8627 1554-8635
    Data From Reference