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  Sequences flanking the core-binding site modulate glucocorticoid receptor structure and activity

Schöne, S., Jurk, M., Helabad, M. B., Dror, I., Lebars, I., Kieffer, B., et al. (2016). Sequences flanking the core-binding site modulate glucocorticoid receptor structure and activity. Nature Communications, 7: 12621. doi:10.1038/ncomms12621.

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Item Permalink: http://hdl.handle.net/11858/00-001M-0000-002D-44F9-A Version Permalink: http://hdl.handle.net/11858/00-001M-0000-002D-44FA-8
Genre: Journal Article

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Schöne, S.1, Author              
Jurk, M.1, Author              
Helabad, M. B., Author
Dror, I., Author
Lebars, I., Author
Kieffer, B., Author
Imhof, P., Author
Rohs, R., Author
Vingron, M.2, Author              
Thomas-Chollier, M., Author
Meijsing, S.1, Author              
Affiliations:
1Mechanisms of Transcriptional Regulation (Sebastiaan H. Meijsing), Dept. of Computational Molecular Biology (Head: Martin Vingron), Max Planck Institute for Molecular Genetics, Max Planck Society, ou_1479641              
2Gene regulation (Martin Vingron), Dept. of Computational Molecular Biology (Head: Martin Vingron), Max Planck Institute for Molecular Genetics, Max Planck Society, ou_1479639              

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 Abstract: The glucocorticoid receptor (GR) binds as a homodimer to genomic response elements, which have particular sequence and shape characteristics. Here we show that the nucleotides directly flanking the core-binding site, differ depending on the strength of GR-dependent activation of nearby genes. Our study indicates that these flanking nucleotides change the three-dimensional structure of the DNA-binding site, the DNA-binding domain of GR and the quaternary structure of the dimeric complex. Functional studies in a defined genomic context show that sequence-induced changes in GR activity cannot be explained by differences in GR occupancy. Rather, mutating the dimerization interface mitigates DNA-induced changes in both activity and structure, arguing for a role of DNA-induced structural changes in modulating GR activity. Together, our study shows that DNA sequence identity of genomic binding sites modulates GR activity downstream of binding, which may play a role in achieving regulatory specificity towards individual target genes.

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Language(s): eng - English
 Dates: 2016-09-012016
 Publication Status: Published in print
 Pages: -
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 Rev. Method: -
 Identifiers: DOI: 10.1038/ncomms12621
ISSN: 2041-1723
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Title: Nature Communications
  Abbreviation : Nat. Commun.
Source Genre: Journal
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Publ. Info: London : Nature Publishing Group
Pages: - Volume / Issue: 7 Sequence Number: 12621 Start / End Page: - Identifier: ISSN: 2041-1723
CoNE: /journals/resource/2041-1723