Abstract
Using a nuclease-dead Cas9 mutant, we show that Cas9 reproducibly induces chromatin accessibility at previously inaccessible genomic loci. Cas9 chromatin opening is sufficient to enable adjacent binding and transcriptional activation by the settler transcription factor retinoic acid receptor at previously unbound motifs. Thus, we demonstrate a new use for Cas9 in increasing surrounding chromatin accessibility to alter local transcription factor binding.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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CRISPR-Associated Proteins / genetics
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CRISPR-Associated Proteins / metabolism*
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CRISPR-Cas Systems*
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Cell Line
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Chromatin / genetics
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Chromatin / metabolism*
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Genetic Loci
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Genome
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Mice
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Mouse Embryonic Stem Cells / metabolism
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Mutation
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Receptors, Retinoic Acid / metabolism*
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Transcriptional Activation*
Substances
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CRISPR-Associated Proteins
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Chromatin
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Receptors, Retinoic Acid