Vincenzo Amodio and Maria Florencia Tevy contributed equally to this work.
Special Issue Techniques
Transactivation in Drosophila of human enhancers by human transcription factors involved in congenital heart diseases†
Article first published online: 11 OCT 2011
Copyright © 2011 Wiley Periodicals, Inc.
Special Issue: Special Issue on Drosophila
Volume 241, Issue 1, pages 190–199, January 2012
How to Cite
Amodio, V., Tevy, M. F., Traina, C., Ghosh, T. K. and Capovilla, M. (2012), Transactivation in Drosophila of human enhancers by human transcription factors involved in congenital heart diseases. Dev. Dyn., 241: 190–199. doi: 10.1002/dvdy.22763
Re-use of this article is permitted in accordance with the Terms and Conditions set out at http://wileyonlinelibrary.com/onlineopen#OnlineOpen_Terms
- Issue published online: 15 DEC 2011
- Article first published online: 11 OCT 2011
- Manuscript Accepted: 10 SEP 2011
- Fondazione Telethon. Grant Number: 3021
- Fondazione San Paolo
- Fondazione Cassa di Risparmio di Cento
- Unknown funding agency
- transcription factor;
- Congenital Heart Disease;
Background: The human transcription factors (TFs) GATA4, NKX2.5 and TBX5 form part of the core network necessary to build a human heart and are involved in Congenital Heart Diseases (CHDs). The human natriuretic peptide precursor A (NPPA) and α-myosin heavy chain 6 (MYH6) genes are downstream effectors involved in cardiogenesis that have been demonstrated to be in vitro targets of such TFs. Results: To study the interactions between these human TFs and their target enhancers in vivo, we overexpressed them in the whole Drosophila cardiac tube using the UAS/GAL4 system. We observed that all three TFs up-regulate their natural target enhancers in Drosophila and cause developmental defects when overexpressed in eyes and wings. Conclusions: A strong potential of the present model might be the development of combinatorial and mutational assays to study the interactions between human TFs and their natural target promoters, which are not easily undertaken in tissue culture cells because of the variability in transfection efficiency, especially when multiple constructs are used. Thus, this novel system could be used to determine in vivo the genetic nature of the human mutant forms of these TFs, setting up a powerful tool to unravel the molecular genetic mechanisms that lead to CHDs. Developmental Dynamics 241:190–199, 2012. © 2011 Wiley Periodicals, Inc.