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Complex gene expression patterns in animal development are generated by the interplay of transcriptional activators and repressors at  cis -regulatory DNA modules (CRMs). How repressors work is not well understood, but often involves interactions with co-repressors. We isolated mutations in the  brakeless  gene in a screen for maternal factors affecting segmentation of the  Drosophila  embryo. Brakeless, also known as Scribbler, or Master of thickveins, is a nuclear protein of unknown function. In  brakeless  embryos, we noted an expanded expression pattern of the  Krüppel (Kr)  and  knirps (kni)  genes. We found that Tailless-mediated repression of  kni  expression is impaired in  brakeless  mutants. Tailless and Brakeless bind each other in vitro and interact genetically. Brakeless is recruited to the  Kr  and  kni  CRMs, and represses transcription when tethered to DNA. This suggests that Brakeless is a novel co-repressor. Orphan nuclear receptors of the Tailless type also interact with Atrophin co-repressors. We show that both  Drosophila  and human Brakeless and Atrophin interact in vitro, and propose that they act together as a co-repressor complex in many developmental contexts. We discuss the possibility that human Brakeless homologs may influence the toxicity of polyglutamine-expanded Atrophin-1, which causes the human neurodegenerative disease dentatorubral-pallidoluysian atrophy (DRPLA).

Drosophila Brakeless Interacts with Atrophin and Is Required for Tailless-Mediated Transcriptional Repression in Early Embryos