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Atrophin controls developmental signaling pathways via interactions with Trithorax-like
Umeå University, Faculty of Medicine, Department of Molecular Biology (Faculty of Medicine). Division of CBRN Security and Defence, FOI-Swedish Defence Research Agency, Umeå, Sweden.
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2017 (English)In: eLIFE, E-ISSN 2050-084X, Vol. 6, e23084Article in journal (Refereed) Published
Abstract [en]

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 Atros critical role in development and disease, relatively little is known about Atros 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.

Place, publisher, year, edition, pages
2017. Vol. 6, e23084
National Category
Developmental Biology
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URN: urn:nbn:se:umu:diva-135291DOI: 10.7554/eLife.23084ISI: 000400260900001OAI: oai:DiVA.org:umu-135291DiVA: diva2:1098544
Available from: 2017-05-24 Created: 2017-05-24 Last updated: 2017-05-24Bibliographically approved

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Karlsson, EdvinStenberg, Per
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CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • harvard1
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
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  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
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