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Nucleic Acids Research Advance Access published online on November 23, 2008
Nucleic Acids Research, doi:10.1093/nar/gkn920
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© 2008 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Gene regulation, Chromatin and Epigenetics

Twist-1 regulates the miR-199a/214 cluster during development

Youn-Bok Lee1, Ioannis Bantounas1, Do-Young Lee1, Leonidas Phylactou2, Maeve A. Caldwell1 and James B. Uney1,*

1The Henry-Wellcome Laboratories for Integrated Neuroscience and Endocrinology, University of Bristol, Dorothy Hodgkin Building, Whitson Street, Bristol, BS1 3NY, UK and 2The Cyprus Institute of Neurology and Genetics, 6 International Airport Avenue PO Box 3462, 1683 Nicosia, Cyprus

*To whom correspondence should be addressed. Tel: +117 3313088; Fax: +117 3313086; Email: james.uney{at}bristol.ac.uk

Received July 20, 2008. Revised October 10, 2008. Accepted November 1, 2008.

MicroRNAs are known to regulate developmental processes but their mechanism of regulation remains largely uncharacterized. We show the transcription factor Twist-1 drives the expression of a 7.9-kb noncoding RNA transcript (from the Dynamin-3 gene intron) that encodes a miR-199a and miR-214 cluster. We also show that knocking down Twist-1 with shRNAs decreased miR-199a/214 levels and that Twist-1 bound an E-Box promoter motif to developmentally regulate the expression of these miRNAs. The expression of HIF-1 (known to mediate Twist-1 transcription), miR-199a and miR-214 was maximal at E12.5 and the miRNAs were expressed specifically in mouse cerebellum, midbrain, nasal process and fore- and hindlimb buds. This study shows the expression of the miR199a/214 cluster is controlled by Twist-1 via an E-Box promoter element and supports a role for these miRNAs as novel intermediates in the pathways controlling the development of specific neural cell populations.


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