Yeung, K;
Boija, A;
Karlsson, E;
Holmqvist, P-H;
Tstskis, Y;
Nisoli, I;
Yap, D;
... McNeill, H; + view all
(2017)
Atrophin controls developmental signaling pathways via interactions with Trithorax-like.
eLIFE
, 6
, Article e23084. 10.7554/eLife.23084.
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Abstract
Mutations in human Atrophin1, a transcriptional corepressor, cause dentatorubral-pallidoluysian atrophy, a neurodegenerative disease. Drosophila Atrophin (Atro) mutants display many phenotypes, including neurodegeneration, segmentation, patterning and planar polarity defects. Despite Atro’s critical role in development and disease, relatively little is known about Atro’s binding partners and downstream targets. We present the first genomic analysis of Atro using ChIP-seq against endogenous Atro. ChIP-seq identified 1300 potential direct targets of Atro including engrailed, and components of the Dpp and Notch signaling pathways. We show that Atro regulates Dpp and Notch signaling in larval imaginal discs, at least partially via regulation of thickveins and fringe. In addition, bioinformatics analyses, sequential ChIP and coimmunoprecipitation experiments reveal that Atro interacts with the Drosophila GAGA Factor, Trithorax-like (Trl), and they bind to the same loci simultaneously. Phenotypic analyses of Trl and Atro clones suggest that Atro is required to modulate the transcription activation by Trl in larval imaginal discs. Taken together, these data indicate that Atro is a major Trl cofactor that functions to moderate developmental gene transcription.
Type: | Article |
---|---|
Title: | Atrophin controls developmental signaling pathways via interactions with Trithorax-like |
Open access status: | An open access version is available from UCL Discovery |
DOI: | 10.7554/eLife.23084 |
Publisher version: | http://doi.org/10.7554/eLife.23084 |
Language: | English |
Additional information: | Copyright © Yeung et al 2017. This article is distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use and redistribution provided that the original author and source are credited. |
UCL classification: | UCL UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Medical Sciences UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Medical Sciences > Div of Infection and Immunity |
URI: | https://discovery.ucl.ac.uk/id/eprint/1557673 |



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