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Molecular and Cellular Biology, November 2005, p. 10029-10039, Vol. 25, No. 22
0270-7306/05/$08.00+0     doi:10.1128/MCB.25.22.10029-10039.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

The Basic Domain of ATH5 Mediates Neuron-Specific Promoter Activity during Retina Development

Dorota Skowronska-Krawczyk,1,2* Lidia Matter-Sadzinski,1,2 Marc Ballivet,2 and Jean-Marc Matter1,2*

University of Lausanne, Eye Hospital Jules Gonin, 15 avenue de France, 1004 Lausanne,1 University of Geneva, Sciences II, Biochemistry Department, 30 quai Ernest-Ansermet, 1211 Geneva, Switzerland2

Received 2 April 2005/ Returned for modification 1 June 2005/ Accepted 17 August 2005

In the developing retina, the gene encoding the ß3 subunit of the neuronal nicotinic receptor, a specific marker of retinal ganglion cells, is under the direct control of the atonal homolog 5 (ATH5) basic helix-loop-helix (bHLH) transcription factor. Although quite short (143 bp in length), the ß3 promoter has the remarkable capacity to discriminate between ATH5 and the other neuronal bHLH proteins expressed in the developing nervous system. We have identified three amino acids within the basic domain that confer specificity to the ATH5 protein. These residues do not mediate direct DNA binding but are required for interaction between ATH5 and chromatin-associated proteins during retina development. When misexpressed in neurons, the myogenic bHLH factor MyoD is also able to activate the ß3 gene. This, however, is achieved not by binding of the protein to the promoter but by dimerization of MyoD with a partner, a process that depends not on the basic domain but on the HLH domain. By sequestering an E-box-binding protein, MyoD relieves the active repression that blocks the ß3 promoter in most neurons. The mechanisms used by bHLH proteins to activate ß3 thus highlight how ATH5 is selected by the ß3 promoter and coordinates the derepression and transcriptional activation of the ß3 gene during the specification of retinal ganglion cells.

* Corresponding author. Mailing address: University of Geneva, Sciences II, Biochemistry Department, 30 quai Ernest-Ansermet, 1211 Geneva, Switzerland. Phone: 41 22 379 6497. Fax: 41 22 379 6495. E-mail for Dorota Skowronska-Krawczyk: Dorota.Skowronska{at}biochem.unige.ch. E-mail for Jean-Marc Matter: Jean-Marc.Matter{at}biochem.unige.ch.

Molecular and Cellular Biology, November 2005, p. 10029-10039, Vol. 25, No. 22
0022-538X/05/$08.00+0     doi:10.1128/MCB.25.22.10029-10039.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Skowronska-Krawczyk, D., Chiodini, F., Ebeling, M., Alliod, C., Kundzewicz, A., Castro, D., Ballivet, M., Guillemot, F., Matter-Sadzinski, L., Matter, J.-M. (2009). Conserved regulatory sequences in Atoh7 mediate non-conserved regulatory responses in retina ontogenesis. Development 136: 3767-3777 [Abstract] [Full Text]  
  • Mao, C.-A., Wang, S. W., Pan, P., Klein, W. H. (2008). Rewiring the retinal ganglion cell gene regulatory network: Neurod1 promotes retinal ganglion cell fate in the absence of Math5. Development 135: 3379-3388 [Abstract] [Full Text]  
  • Hernandez, J., Matter-Sadzinski, L., Skowronska-Krawczyk, D., Chiodini, F., Alliod, C., Ballivet, M., Matter, J.-M. (2007). Highly Conserved Sequences Mediate the Dynamic Interplay of Basic Helix-Loop-Helix Proteins Regulating Retinogenesis. J. Biol. Chem. 282: 37894-37905 [Abstract] [Full Text]  


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