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Coolen, M. ; Thieffry, D.* ; Drivenes, O.* ; Becker, T.S.* ; Bally-Cuif, L.

MiR-9 controls the timing of neurogenesis through the direct inhibition of antagonistic factors.

Dev. Cell 22, 1052-1064 (2012)
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Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
The timing of commitment and cell-cycle exit within progenitor populations during neurogenesis is a fundamental decision that impacts both the number and identity of neurons produced during development. We show here that microRNA-9 plays a key role in this process through the direct inhibition of targets with antagonistic functions. Across the ventricular zone of the developing zebrafish hindbrain, miR-9 expression occurs at a range of commitment stages. Abrogating miR-9 function transiently delays cell-cycle exit, leading to the increased generation of late-born neuronal populations. Target protection analyses in vivo identify the progenitor-promoting genes her6 and zic5 and the cell-cycle exit-promoting gene elavl3/HuC as sequential targets of miR-9 as neurogenesis proceeds. We propose that miR-9 activity generates an ambivalent progenitor state poised to respond to both progenitor maintenance and commitment cues, which may be necessary to adjust neuronal production to local extrinsic signals during late embryogenesis.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter RNA-BINDING PROTEINS; MIDBRAIN-HINDBRAIN BOUNDARY; EMBRYONIC-DEVELOPMENT; MICRORNA EXPRESSION; NEURAL PROGENITORS; MESSENGER-RNA; NEURONAL DIFFERENTIATION; REGULATES NEUROGENESIS; TRANSCRIPTION FACTORS; ZEBRAFISH HINDBRAIN
Sprache
Veröffentlichungsjahr 2012
HGF-Berichtsjahr 2012
ISSN (print) / ISBN 1534-5807
e-ISSN 1878-1551
Zeitschrift Developmental Cell
Quellenangaben Band: 22, Heft: 5, Seiten: 1052-1064 Artikelnummer: , Supplement: ,
Verlag Elsevier
Begutachtungsstatus Peer reviewed
POF Topic(s) 30204 - Cell Programming and Repair
Forschungsfeld(er) Genetics and Epidemiology
PSP-Element(e) G-500500-001
PubMed ID 22595676
Scopus ID 84860901706
Erfassungsdatum 2012-06-14