miR-200 family controls late steps of postnatal forebrain neurogenesis via Zeb2 inhibition

During neurogenesis, generation, migration and integration of the correct numbers of each neuron sub-type depends on complex molecular interactions in space and time. MicroRNAs represent a key control level allowing the flexibility and stability needed for this process. Insight into the role of this...

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Main Authors: Beclin, Christophe, Follert, Philipp, Stappers, Elke, Barral, Serena, Nathalie, Coré, de Chevigny, Antoine, Magnone, Virginie, Lebrigand, Kévin, Bissels, Ute, Huylebroeck, Danny, Bosio, Andreas, Barbry, Pascal, Seuntjens, Eve, Cremer, Harold
Format: Online
Language:English
Published: Nature Publishing Group 2016
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5073329/
id pubmed-5073329
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spelling pubmed-50733292016-10-26 miR-200 family controls late steps of postnatal forebrain neurogenesis via Zeb2 inhibition Beclin, Christophe Follert, Philipp Stappers, Elke Barral, Serena Nathalie, Coré de Chevigny, Antoine Magnone, Virginie Lebrigand, Kévin Bissels, Ute Huylebroeck, Danny Bosio, Andreas Barbry, Pascal Seuntjens, Eve Cremer, Harold Article During neurogenesis, generation, migration and integration of the correct numbers of each neuron sub-type depends on complex molecular interactions in space and time. MicroRNAs represent a key control level allowing the flexibility and stability needed for this process. Insight into the role of this regulatory pathway in the brain is still limited. We performed a sequential experimental approach using postnatal olfactory bulb neurogenesis in mice, starting from global expression analyses to the investigation of functional interactions between defined microRNAs and their targets. Deep sequencing of small RNAs extracted from defined compartments of the postnatal neurogenic system demonstrated that the miR-200 family is specifically induced during late neuronal differentiation stages. Using in vivo strategies we interfered with the entire miR-200 family in loss- and gain-of-function settings, showing a role of miR-200 in neuronal maturation. This function is mediated by targeting the transcription factor Zeb2. Interestingly, so far functional interaction between miR-200 and Zeb2 has been exclusively reported in cancer or cultured stem cells. Our data demonstrate that this regulatory interaction is also active during normal neurogenesis. Nature Publishing Group 2016-10-21 /pmc/articles/PMC5073329/ /pubmed/27767083 http://dx.doi.org/10.1038/srep35729 Text en Copyright © 2016, The Author(s) http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Beclin, Christophe
Follert, Philipp
Stappers, Elke
Barral, Serena
Nathalie, Coré
de Chevigny, Antoine
Magnone, Virginie
Lebrigand, Kévin
Bissels, Ute
Huylebroeck, Danny
Bosio, Andreas
Barbry, Pascal
Seuntjens, Eve
Cremer, Harold
spellingShingle Beclin, Christophe
Follert, Philipp
Stappers, Elke
Barral, Serena
Nathalie, Coré
de Chevigny, Antoine
Magnone, Virginie
Lebrigand, Kévin
Bissels, Ute
Huylebroeck, Danny
Bosio, Andreas
Barbry, Pascal
Seuntjens, Eve
Cremer, Harold
miR-200 family controls late steps of postnatal forebrain neurogenesis via Zeb2 inhibition
author_facet Beclin, Christophe
Follert, Philipp
Stappers, Elke
Barral, Serena
Nathalie, Coré
de Chevigny, Antoine
Magnone, Virginie
Lebrigand, Kévin
Bissels, Ute
Huylebroeck, Danny
Bosio, Andreas
Barbry, Pascal
Seuntjens, Eve
Cremer, Harold
author_sort Beclin, Christophe
title miR-200 family controls late steps of postnatal forebrain neurogenesis via Zeb2 inhibition
title_short miR-200 family controls late steps of postnatal forebrain neurogenesis via Zeb2 inhibition
title_full miR-200 family controls late steps of postnatal forebrain neurogenesis via Zeb2 inhibition
title_fullStr miR-200 family controls late steps of postnatal forebrain neurogenesis via Zeb2 inhibition
title_full_unstemmed miR-200 family controls late steps of postnatal forebrain neurogenesis via Zeb2 inhibition
title_sort mir-200 family controls late steps of postnatal forebrain neurogenesis via zeb2 inhibition
description During neurogenesis, generation, migration and integration of the correct numbers of each neuron sub-type depends on complex molecular interactions in space and time. MicroRNAs represent a key control level allowing the flexibility and stability needed for this process. Insight into the role of this regulatory pathway in the brain is still limited. We performed a sequential experimental approach using postnatal olfactory bulb neurogenesis in mice, starting from global expression analyses to the investigation of functional interactions between defined microRNAs and their targets. Deep sequencing of small RNAs extracted from defined compartments of the postnatal neurogenic system demonstrated that the miR-200 family is specifically induced during late neuronal differentiation stages. Using in vivo strategies we interfered with the entire miR-200 family in loss- and gain-of-function settings, showing a role of miR-200 in neuronal maturation. This function is mediated by targeting the transcription factor Zeb2. Interestingly, so far functional interaction between miR-200 and Zeb2 has been exclusively reported in cancer or cultured stem cells. Our data demonstrate that this regulatory interaction is also active during normal neurogenesis.
publisher Nature Publishing Group
publishDate 2016
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5073329/
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