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

Author:

Wang YupuORCID,Zhang Ruiling,Huang Sihao,Valverde Parisa Tajalli Tehrani,Lobb-Rabe Meike,Ashley James,Venkatasubramanian Lalanti,Carrillo Robert A.ORCID

Abstract

AbstractNeuronal 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.

Funder

U.S. Department of Health & Human Services | NIH | National Institute of Neurological Disorders and Stroke

NSF | BIO | Division of Integrative Organismal Systems

U.S. Department of Health & Human Services | NIH | Eunice Kennedy Shriver National Institute of Child Health and Human Development

Publisher

Springer Science and Business Media LLC

Subject

General Physics and Astronomy,General Biochemistry, Genetics and Molecular Biology,General Chemistry,Multidisciplinary

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