title: Cas9 Functionally Opens Chromatin.
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.
authors.affiliation: Division of Genetics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, United States of America.|Computer Science and Artificial Intelligence Laboratory, Massachusetts Institute of Technology, Cambridge, Massachusetts, United States of America.
authors.forename: Amira A
authors.initials: AA
authors.lastname: Barkal
authors.affiliation: Division of Genetics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, United States of America.|Computer Science and Artificial Intelligence Laboratory, Massachusetts Institute of Technology, Cambridge, Massachusetts, United States of America.
authors.forename: Sharanya
authors.initials: S
authors.lastname: Srinivasan
authors.affiliation: Computer Science and Artificial Intelligence Laboratory, Massachusetts Institute of Technology, Cambridge, Massachusetts, United States of America.
authors.forename: Tatsunori
authors.initials: T
authors.lastname: Hashimoto
authors.affiliation: Computer Science and Artificial Intelligence Laboratory, Massachusetts Institute of Technology, Cambridge, Massachusetts, United States of America.|Department of Stem Cell and Regenerative Biology, Harvard University and Harvard Medical School, 7 Divinity Avenue, Cambridge, Massachusetts, United States of America.
authors.forename: David K
authors.initials: DK
authors.lastname: Gifford
authors.affiliation: Division of Genetics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, United States of America.
authors.forename: Richard I
authors.initials: RI
authors.lastname: Sherwood
mesh_terms: D000818:Animals; D064130:CRISPR-Associated Proteins / Q000235:genetics / Q000378:metabolism*; D064113:CRISPR-Cas Systems; D002460:Cell Line; D002843:Chromatin / Q000235:genetics / Q000378:metabolism*; D056426:Genetic Loci; D016678:Genome; D051379:Mice; D000066450:Mouse Embryonic Stem Cells / Q000378:metabolism; D009154:Mutation; D018168:Receptors, Retinoic Acid / Q000378:metabolism*; D015533:Transcriptional Activation
chemical_list: D064130:CRISPR-Associated Proteins; D002843:Chromatin; D018168:Receptors, Retinoic Acid