UMMS Affiliation
Department of Molecular, Cell, and Cancer Biology
Publication Date
2016-08-16
Document Type
Article
Disciplines
Molecular and Cellular Neuroscience
Abstract
Neuronal injury triggers robust responses from glial cells, including altered gene expression and enhanced phagocytic activity to ensure prompt removal of damaged neurons. The molecular underpinnings of glial responses to trauma remain unclear. Here, we find that the evolutionarily conserved insulin-like signaling (ILS) pathway promotes glial phagocytic clearance of degenerating axons in adult Drosophila. We find that the insulin-like receptor (InR) and downstream effector Akt1 are acutely activated in local ensheathing glia after axotomy and are required for proper clearance of axonal debris. InR/Akt1 activity, it is also essential for injury-induced activation of STAT92E and its transcriptional target draper, which encodes a conserved receptor essential for glial engulfment of degenerating axons. Increasing Draper levels in adult glia partially rescues delayed clearance of severed axons in glial InR-inhibited flies. We propose that ILS functions as a key post-injury communication relay to activate glial responses, including phagocytic activity.
DOI of Published Version
10.1016/j.celrep.2016.07.022
Source
Cell Rep. 2016 Aug 16;16(7):1838-50. doi: 10.1016/j.celrep.2016.07.022. Epub 2016 Aug 4. Link to article on publisher's site
Journal/Book/Conference Title
Cell reports
Related Resources
PubMed ID
27498858
Repository Citation
Musashe, Derek T.; Purice, Maria D.; Speese, Sean D.; Doherty, Johnna E.; and Logan, Mary A., "Insulin-like Signaling Promotes Glial Phagocytic Clearance of Degenerating Axons through Regulation of Draper" (2016). Open Access Articles. 2926.
https://escholarship.umassmed.edu/oapubs/2926
Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 License.