ArticleMolecular and cellular biology2005
The basic domain of ATH5 mediates neuron-specific promoter activity during retina development.
Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 16 citations in OpenAlex.
- Functional Characterization of an In-Frame Deletion in the Basic Domain of the Retinal Transcription Factor ATOH7.International journal of molecular sciences · 2022Article
- Prosurvival long noncoding RNAeLife · 2017Article
- Biasing amacrine subtypes in the Atoh7 lineage through expression of Barhl2.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- In vivo neuronal subtype-specific targets of Atoh1 (Math1) in dorsal spinal cord.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Integrating computational biology and forward genetics in Drosophila.PLoS genetics · 2009Article
- Context dependence of proneural bHLH proteins.Current opinion in genetics & development · 2008Review
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Authors and funding
4 authors at 1 institution in 1 country.
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Abstract
In the developing retina, the gene encoding the beta3 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 beta3 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 beta3 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 beta3 promoter in most neurons. The mechanisms used by bHLH proteins to activate beta3 thus highlight how ATH5 is selected by the beta3 promoter and coordinates the derepression and transcriptional activation of the beta3 gene during the specification of retinal ganglion cells.
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