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Open Access Green as soon as Postprint is submitted to ZB.
MiR-9 controls the timing of neurogenesis through the direct inhibition of antagonistic factors.
Dev. Cell 22, 1052-1064 (2012)
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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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
RNA-BINDING PROTEINS; MIDBRAIN-HINDBRAIN BOUNDARY; EMBRYONIC-DEVELOPMENT; MICRORNA EXPRESSION; NEURAL PROGENITORS; MESSENGER-RNA; NEURONAL DIFFERENTIATION; REGULATES NEUROGENESIS; TRANSCRIPTION FACTORS; ZEBRAFISH HINDBRAIN
ISSN (print) / ISBN
1534-5807
e-ISSN
1878-1551
Journal
Developmental Cell
Quellenangaben
Volume: 22,
Issue: 5,
Pages: 1052-1064
Publisher
Elsevier
Non-patent literature
Publications
Reviewing status
Peer reviewed
Institute(s)
Institute of Developmental Genetics (IDG)