Glial Draper signaling triggers cross-neuron plasticity in bystander neurons after neuronal cell death in Drosophila

Yupu Wang (), Ruiling Zhang, Sihao Huang, Parisa Tajalli Tehrani Valverde, Meike Lobb-Rabe, James Ashley, Lalanti Venkatasubramanian and Robert A. Carrillo ()
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Yupu Wang: University of Chicago
Ruiling Zhang: University of Chicago
Sihao Huang: University of Chicago
Parisa Tajalli Tehrani Valverde: University of Chicago
Meike Lobb-Rabe: University of Chicago
James Ashley: University of Chicago
Lalanti Venkatasubramanian: University of Cambridge
Robert A. Carrillo: University of Chicago

Nature Communications, 2023, vol. 14, issue 1, 1-15

Abstract: 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.

Date: 2023
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DOI: 10.1038/s41467-023-40142-y

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