Damage in the nervous system induces a stereotypical response that is mediated by glial cells. Here, we use the eye disc to explore the mechanisms involved in promoting glial cell response after neural injuries. We demonstrate that eye glia cells rapidly respond to neuronal injury by increasing in number and undergoing morphological changes, which grant them phagocytic abilities.We found that this glial response is controlled by the activity of the long-range signalling pathways, decapentaplegic (dpp) and hedgehog (hh). These pathways are activated in the damaged region and their functions are necessary for inducing glial cell proliferation and migration to the eye discs. The latter of these two processes depends on the function of the JNK pathway, which is cooperatively activated by dpp and hh signalling.3
Damage in the nervous system induces a stereotypical response that is mediated by glial cells. Here, we use the eye disc of Drosophila melanogaster as a model to explore the mechanisms involved in promoting glial cell response after neuronal cell death induction. We demonstrate that these cells rapidly respond to neuronal apoptosis by increasing in number and undergoing morphological changes, which will ultimately grant them phagocytic abilities. We found that this glial response is controlled by the activity of Decapentaplegic (Dpp) and Hedgehog (Hh) signalling pathways. These pathways are activated after cell death induction, and their functions are necessary to induce glial cell proliferation and migration to the eye discs. The latter of these 2 processes depend on the function of the c-Jun N-terminal kinase (JNK) pathway, which is activated by Dpp signalling. We also present evidence that a similar mechanism controls glial response upon apoptosis induction in the leg discs, suggesting that our results uncover a mechanism that might be involved in controlling glial cells response to neuronal cell death in different regions of the peripheral nervous system (PNS).
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