Cas9 Functionally Opens Chromatin

被引：25

作者：

Barkal, Amira A. ^{[1
,2
,3
]}

Srinivasan, Sharanya ^{[1
,2
,3
]}

Hashimoto, Tatsunori ^{[3
]}

Gifford, David K. ^{[3
,4
,5
]}

Sherwood, Richard I. ^{[1
,2
]}

机构：

[1] Brigham & Womens Hosp, Dept Med, Div Genet, 75 Francis St, Boston, MA 02115 USA

[2] Harvard Univ, Sch Med, Boston, MA USA

[3] MIT, Comp Sci & Artificial Intelligence Lab, 77 Massachusetts Ave, Cambridge, MA 02139 USA

[4] Harvard Univ, Dept Stem Cell & Regenerat Biol, 7 Divin Ave, Cambridge, MA 02138 USA

[5] Harvard Univ, Sch Med, 7 Divin Ave, Cambridge, MA 02138 USA

来源：

PLOS ONE | 2016年 / 11卷 / 03期

基金：

美国国家卫生研究院;

关键词：

HUMAN GENOME; TARGET DNA; RNA; BINDING; CRISPR; GENES; TRANSPOSITION; TRANSCRIPTION; ENDONUCLEASE; ELEMENT;

D O I：

10.1371/journal.pone.0152683

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

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.

引用

页数：8

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