miR-9 controls the timing of neurogenesis through the direct inhibition of antagonistic factors.
Identifieur interne : 000168 ( France/Analysis ); précédent : 000167; suivant : 000169miR-9 controls the timing of neurogenesis through the direct inhibition of antagonistic factors.
Auteurs : Marion Coolen [France] ; Denis Thieffry [France] ; Yvind Drivenes [Norvège] ; Thomas S. Becker [Norvège] ; Laure Bally-Cuif [France]Source :
- Developmental Cell [ 1534-5807 ] ; 2012-05-15.
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.
Url:
DOI: 10.1016/j.devcel.2012.03.003
Affiliations:
Links toward previous steps (curation, corpus...)
- to stream Hal, to step Corpus: 000184
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- to stream Hal, to step Checkpoint: 000114
- to stream Main, to step Merge: 001C26
- to stream Main, to step Curation: 001C16
- to stream Main, to step Exploration: 001C16
- to stream France, to step Extraction: 000168
Links to Exploration step
Hal:hal-00732227Le document en format XML
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<front><div type="abstract" xml:lang="en"> <p>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.</p>
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EXPLOR_STEP=$WICRI_ROOT/Sante/explor/SrasV1/Data/France/Analysis
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HfdSelect -h $EXPLOR_AREA/Data/France/Analysis/biblio.hfd -nk 000168 | SxmlIndent | more
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{{Explor lien |wiki= Sante |area= SrasV1 |flux= France |étape= Analysis |type= RBID |clé= Hal:hal-00732227 |texte= miR-9 controls the timing of neurogenesis through the direct inhibition of antagonistic factors. }}
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