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Cell Rep. 2018 Oct 16;25(3):737-748.e4. doi: 10.1016/j.celrep.2018.09.050.

Insights into Bidirectional Gene Expression Control Using the Canonical GAL1/GAL10 Promoter.

Author information

1
Department of Molecular Cellular and Developmental Biology, Yale University, 219 Prospect Street, New Haven, CT 06511, USA; Systems Biology Institute, Yale University, 850 West Campus Drive, West Haven, CT 06516, USA.
2
Systems Biology Institute, Yale University, 850 West Campus Drive, West Haven, CT 06516, USA; Interdepartmental Program in Computational Biology and Bioinformatics, Yale University, 300 George Street, Suite 501, New Haven, CT 06511, USA.
3
Department of Molecular Cellular and Developmental Biology, Yale University, 219 Prospect Street, New Haven, CT 06511, USA; Systems Biology Institute, Yale University, 850 West Campus Drive, West Haven, CT 06516, USA; Interdepartmental Program in Computational Biology and Bioinformatics, Yale University, 300 George Street, Suite 501, New Haven, CT 06511, USA; Department of Physics, Yale University, 217 Prospect Street, New Haven, CT 06511, USA. Electronic address: murat.acar@yale.edu.

Abstract

Despite advances made in understanding the effects of promoter structure on transcriptional activity, limited knowledge exists regarding the role played by chromatin architecture in transcription. Previous work hypothesized that transcription from the bidirectional GAL1/GAL10 promoter is controlled through looping of its UAS region around a nonstandard nucleosome. Here, by editing the GAL1/GAL10 promoter at high resolution, we provide insights into bidirectional expression control. We demonstrate that the first and fourth Gal4 binding sites within the UAS do not functionally contribute to promoter activation. Instead, these sites, along with nearby regulatory regions, contribute to the directional regulation of gene expression. Furthermore, Gal4 binding to the third binding site is critical for gene expression, while binding to the other three sites is not sufficient for transcriptional activation. Because the GAL1/GAL10 UAS can activate gene expression in many eukaryotes, the regulatory mechanism presented is expected to operate broadly across the eukaryotic clade.

KEYWORDS:

CRISPR; GAL1 promoter; GAL1/10; GAL10 promoter; Gal4; Gal4 binding site; UAS; bidirectional promoter; gene regulation; nucleosome

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