Atrophin (Atro, also known as Grunge) is a transcriptional corepressor. Mutation of a mammalian Atro homolog, Atrophin-1, causes a neurodegenerative disease called dentatorubral-pallidoluysian atrophy in humans, while mutation of the second mammalian Atro homolog, Atrophin-2, causes severe developmental defects. Although Drosophila Atro mutants have a large range of phenotypes including neurodegeneration, segmentation and planar polarity defects, very little is known about Atro’s binding partners and downstream targets. We present the first genomic analysis of Atro using ChIP-seq against Atro. Our Atro ChIP-seq identified 1300 potential targets of Atro; these include engrailed, and components of the dpp and Notch signaling pathways. Using Atro mutant clones, we show that Atro regulates dpp signaling and the expression of Engrailed in imaginal discs. Interestingly, Atro mutant imaginal disc clones have similar phenotypes to the ones caused by loss of Notch signaling. In addition, our bioinformatic analyses, sequential ChIP and coimmunoprecipitation experiments show that Atro and Trithorax-like (Trl, Drosophila GAGA factor) physically interact and bind to the same loci. Atro and Trl also interact genetically. We propose that Atro and Trl function together as a complex to regulate transcription.