ArticleProceedings of the National Academy of Sciences of the United States of America2014
DRK/DOS/SOS converge with Crk/Mbc/dCed-12 to activate Rac1 during glial engulfment of axonal debris.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 40 citations in OpenAlex.
- Neuron-to-glia and glia-to-glia signaling directs critical period experience-dependent synapse pruning.Frontiers in cell and developmental biology · 2025Review
- Glial Regulation of Circuit Wiring, Firing, and Expiring in theCold Spring Harbor perspectives in biology · 2024Review
- A Pvr-AP-1-Mmp1 signaling pathway is activated in astrocytes upon traumatic brain injury.eLife · 2024Article
- Experience-dependent glial pruning of synaptic glomeruli during the critical period.Scientific reports · 2024Article
- Glial Draper signaling triggers cross-neuron plasticity in bystander neurons after neuronal cell death in Drosophila.Nature communications · 2023Article
- LC3-associated phagocytosis promotes glial degradation of axon debris after injury in Drosophila models.Nature communications · 2023Article
- Glial Draper signaling triggers cross-neuron plasticity in bystander neurons after neuronal cell death.bioRxiv : the preprint server for biology · 2023Article
- The phagocytic cyst cells inScience advances · 2022Article
- Glia actively sculpt sensory neurons by controlled phagocytosis to tune animal behavior.eLife · 2021Article
- Neuronal fragile X mental retardation protein activates glial insulin receptor mediated PDF-Tri neuron developmental clearance.Nature communications · 2021Article
- Engulfed by Glia: Glial Pruning in Development, Function, and Injury across Species.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Review
- Phagocyte Responses to Cell Death in Flies.Cold Spring Harbor perspectives in biology · 2020Review
- Spatial control of Draper receptor signaling initiates apoptotic cell engulfment.The Journal of cell biology · 2018Article
- Phosphorylation of SOS1 on tyrosine 1196 promotes its RAC GEF activity and contributes to BCR-ABL leukemogenesis.Leukemia · 2018Article
- A noveleLife · 2017Article
- Protein phosphatase 4 coordinates glial membrane recruitment and phagocytic clearance of degenerating axons in Drosophila.Cell death & disease · 2017Article
- Axon degeneration induces glial responses through Draper-TRAF4-JNK signalling.Nature communications · 2017Article
- Scrambled Eggs: Apoptotic Cell Clearance by Non-Professional Phagocytes in theFrontiers in immunology · 2017Review
- Article
- Drosophila Central Nervous System Glia.Cold Spring Harbor perspectives in biology · 2015Review
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Nervous system injury or disease leads to activation of glia, which govern postinjury responses in the nervous system. Axonal injury in Drosophila results in transcriptional up-regulation of the glial engulfment receptor Draper; there is extension of glial membranes to the injury site (termed activation), and then axonal debris is internalized and degraded. Loss of the small GTPase Rac1 from glia completely suppresses glial responses to injury, but upstream activators remain poorly defined. Loss of the Rac guanine nucleotide exchange factor (GEF) Crk/myoblast city (Mbc)/dCed-12 has no effect on glial activation, but blocks internalization and degradation of debris. Here we show that the signaling molecules downstream of receptor kinase (DRK) and daughter of sevenless (DOS) (mammalian homologs, Grb2 and Gab2, respectively) and the GEF son of sevenless (SOS) (mammalian homolog, mSOS) are required for efficient activation of glia after axotomy and internalization/degradation of axonal debris. At the earliest steps of glial activation, DRK/DOS/SOS function in a partially redundant manner with Crk/Mbc/dCed-12, with blockade of both complexes strongly suppressing all glial responses, similar to loss of Rac1. This work identifies DRK/DOS/SOS as the upstream Rac GEF complex required for glial responses to axonal injury, and demonstrates a critical requirement for multiple GEFs in efficient glial activation after injury and internalization/degradation of axonal debris.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.