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di Giaimo, R. ; Durovic, T. ; Barquin, P.* ; Kociaj, A. ; Lepko, T. ; Aschenbroich, S. ; Breunig, C. ; Irmler, M. ; Cernilogar, F.M.* ; Schotta, G.* ; Barbosa, J.S. ; Trümbach, D. ; Baumgart, E.V. ; Neuner, A.M. ; Beckers, J. ; Wurst, W. ; Stricker, S.H. ; Ninkovic, J.

The aryl hydrocarbon receptor pathway defines the time frame for restorative neurogenesis.

Cell Rep. 25, 3241-3251.e5 (2018)
Publ. Version/Full Text Research data DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
Zebrafish have a high capacity to replace lost neurons after brain injury. New neurons involved in repair are generated by a specific set of glial cells, known as ependymoglial cells. We analyze changes in the transcriptome of ependymoglial cells and their progeny after injury to infer the molecular pathways governing restorative neurogenesis. We identify the aryl hydrocarbon receptor (AhR) as a regulator of ependymoglia differentiation toward post-mitotic neurons. In vivo imaging shows that high AhR signaling promotes the direct conversionof a specific subset of ependymoglia into post-mitotic neurons, while low AhR signaling promotes ependymoglial proliferation. Interestingly, we observe the inactivation of AhR signaling shortly after injury followed by a return to the basal levels 7 days post injury. Interference with timely AhR regulation after injury leads to aberrant restorative neurogenesis. Taken together, we identify AhR signaling as a crucial regulator of restorative neurogenesis timing in the zebrafish brain.
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Publication type Article: Journal article
Document type Scientific Article
Keywords Aryl Hydrocarbon Receptor ; Direct Conversion ; Live Imaging ; Neurogenesis ; Regeneration ; Zebrafish; Neural Stem-cells; Neuronal Regeneration; Glial-cells; Adult Brain; Zebrafish; Expression; Ligands; Activation; Injury; Roles
Language english
Publication Year 2018
HGF-reported in Year 2018
ISSN (print) / ISBN 2211-1247
e-ISSN 2211-1247
Journal Cell Reports
Quellenangaben Volume: 25, Issue: 12, Pages: 3241-3251.e5 Article Number: , Supplement: ,
Publisher Cell Press
Publishing Place 50 Hampshire St, Floor 5, Cambridge, Ma 02139 Usa
Reviewing status Peer reviewed
Institute(s) Institute of Stem Cell Research (ISF)
Institute of Experimental Genetics (IEG)
Institute of Developmental Genetics (IDG)
Institute of Diabetes and Obesity (IDO)
POF-Topic(s) 30204 - Cell Programming and Repair
30201 - Metabolic Health
30502 - Diabetes: Pathophysiology, Prevention and Therapy
30504 - Mechanisms of Genetic and Environmental Influences on Health and Disease
Research field(s) Stem Cell and Neuroscience
Genetics and Epidemiology
Helmholtz Diabetes Center
PSP Element(s) G-500800-001
G-500600-004
G-500500-001
G-502294-002
G-500500-007
G-500500-006
G-500600-006
DOI 10.1016/j.celrep.2018.11.055
WOS ID WOS:000453826600002
Scopus ID 85057625691
PubMed ID 30566853
Erfassungsdatum 2018-12-20
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