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

TitlemiR-9 controls the timing of neurogenesis through the direct inhibition of antagonistic factors.
Publication TypeJournal Article
Year of Publication2012
AuthorsCoolen M, Thieffry D, Drivenes Ø, Becker TS, Bally-Cuif L
JournalDevelopmental cell
Volume22
Issue5
Pagination1052-64
Date Published2012 May 15
ISSN1878-1551
KeywordsAlanine, Animals, Azepines, Basic Helix-Loop-Helix Transcription Factors, Cell Cycle, Cell Differentiation, DNA-Binding Proteins, ELAV Proteins, ELAV-Like Protein 3, MicroRNAs, Neurogenesis, Neurons, Zebrafish, Zebrafish Proteins
Abstract

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.

DOI10.1016/j.devcel.2012.03.003
Alternate JournalDev. Cell


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