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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)
Verlagsversion Forschungsdaten 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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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter 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
Sprache englisch
Veröffentlichungsjahr 2018
HGF-Berichtsjahr 2018
ISSN (print) / ISBN 2211-1247
e-ISSN 2211-1247
Zeitschrift Cell Reports
Quellenangaben Band: 25, Heft: 12, Seiten: 3241-3251.e5 Artikelnummer: , Supplement: ,
Verlag Cell Press
Verlagsort 50 Hampshire St, Floor 5, Cambridge, Ma 02139 Usa
Begutachtungsstatus Peer reviewed
Institut(e) 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
Forschungsfeld(er) Stem Cell and Neuroscience
Genetics and Epidemiology
Helmholtz Diabetes Center
PSP-Element(e) 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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