ArticleGenetics2006
Genetic interactions among scribbler, Atrophin and groucho in Drosophila uncover links in transcriptional repression.
Article in Genetics, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 14 citations in OpenAlex.
- Regulation of Hippo signaling by Atrophin in the developing Drosophila wing.Development (Cambridge, England) · 2026Article
- Tissue-specific enhancer repression through molecular integration of cell signaling inputs.PLoS genetics · 2017Article
- Atrophin controls developmental signaling pathways via interactions with Trithorax-like.eLife · 2017Article
- Atrophin proteins: an overview of a new class of nuclear receptor corepressors.Nuclear receptor signaling · 2008Review
- Drosophila brakeless interacts with atrophin and is required for tailless-mediated transcriptional repression in early embryos.PLoS biology · 2007Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
In eukaryotes, the ability of DNA-binding proteins to act as transcriptional repressors often requires that they recruit accessory proteins, known as corepressors, which provide the activity responsible for silencing transcription. Several of these factors have been identified, including the Groucho (Gro) and Atrophin (Atro) proteins in Drosophila. Here we demonstrate strong genetic interactions between gro and Atro and also with mutations in a third gene, scribbler (sbb), which encodes a nuclear protein of unknown function. We show that mutations in Atro and Sbb have similar phenotypes, including upregulation of the same genes in imaginal discs, which suggests that Sbb cooperates with Atro to provide repressive activity. Comparison of gro and Atro/sbb mutant phenotypes suggests that they do not function together, but instead that they may interact with the same transcription factors, including Engrailed and C15, to provide these proteins with maximal repressive activity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.