DLK regulates a distinctive transcriptional regeneration program after peripheral nerve injury
- Authors
- Shin, Jung Eun; Ha, Hongseok; Kim, Yoon Ki; Cho, Yongcheol; DiAntonio, Aaron
- Issue Date
- 7월-2019
- Publisher
- ACADEMIC PRESS INC ELSEVIER SCIENCE
- Keywords
- Dual leucine zipper kinase; Conditioning injury; Axon regeneration; Neuroinflammation; Neurodegeneration; Pain
- Citation
- NEUROBIOLOGY OF DISEASE, v.127, pp.178 - 192
- Indexed
- SCIE
SCOPUS
- Journal Title
- NEUROBIOLOGY OF DISEASE
- Volume
- 127
- Start Page
- 178
- End Page
- 192
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/64592
- DOI
- 10.1016/j.nbd.2019.02.001
- ISSN
- 0969-9961
- Abstract
- Following damage to a peripheral nerve, injury signaling pathways converge in the cell body to generate transcriptional changes that support axon regeneration. Here, we demonstrate that dual leucine zipper kinase (DLK), a central regulator of injury responses including axon regeneration and neuronal apoptosis, is required for the induction of the pro-regenerative transcriptional program in response to peripheral nerve injury. Using a sensory neuron-conditional DLK knockout mouse model, we show a time course for the dependency of gene expression changes on the DLK pathway after sciatic nerve injury. Gene ontology analysis reveals that DLK-dependent gene sets are enriched for specific functional annotations such as ion transport and immune response. A series of comparative analyses shows that the DLK-dependent transcriptional program is distinct from that promoted by the importin-dependent retrograde signaling pathway, while it is partially shared between PNS and CNS injury responses. We suggest that DLK-dependency might provide a selective filter for regeneration-associated genes among the injury-responsive transcriptome.
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Collections - Graduate School > Department of Life Sciences > 1. Journal Articles
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