ArticleMolecular and cellular biology2012
Essential roles of Da transactivation domains in neurogenesis and in E(spl)-mediated repression.
Article in Molecular and cellular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- The Id protein Extramacrochaetae restrains the E protein Daughterless to regulate Notch, Rap1, and Sevenless within the R7 equivalence group of the Drosophila eye.Biology open · 2024Article
- The CDK8 Complex and Proneural Proteins Together Drive Neurogenesis from a Mesodermal Lineage.Current biology : CB · 2017Article
- Article
- Introducing Pitt-Hopkins syndrome-associated mutations of TCF4 to Drosophila daughterless.Biology open · 2015Article
- bHLH proteins involved in Drosophila neurogenesis are mutually regulated at the level of stability.Nucleic acids research · 2015Article
- A re-examination of the selection of the sensory organ precursor of the bristle sensilla of Drosophila melanogaster.PLoS genetics · 2015Article
- Translational Control of Serrate Expression in Drosophila Cells.In vivo (Athens, Greece)Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
E proteins are a special class of basic helix-loop-helix (bHLH) proteins that heterodimerize with many bHLH activators to regulate developmental decisions, such as myogenesis and neurogenesis. Daughterless (Da) is the sole E protein in Drosophila and is ubiquitously expressed. We have characterized two transcription activation domains (TADs) in Da, called activation domain 1 (AD1) and loop-helix (LH), and have evaluated their roles in promoting peripheral neurogenesis. In this context, Da heterodimerizes with proneural proteins, such as Scute (Sc), which is dynamically expressed and also contributes a TAD. We found that either one of the Da TADs in the Da/Sc complex is sufficient to promote neurogenesis, whereas the Sc TAD is incapable of doing so. Besides its transcriptional activation role, the Da AD1 domain serves as an interaction platform for E(spl) proteins, bHLH-Orange family repressors which antagonize Da/Sc function. We show that the E(spl) Orange domain is needed for this interaction and strongly contributes to the antiproneural activity of E(spl) proteins. We present a mechanistic model on the interplay of these bHLH factors in the context of neural fate assignment.
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