Gilbert Luke A, Horlbeck Max A, Adamson Britt, Villalta Jacqueline E, Chen Yuwen, Whitehead Evan H, Guimaraes Carla, Panning Barbara, Ploegh Hidde L, Bassik Michael C, Qi Lei S, Kampmann Martin, Weissman Jonathan S
Department of Cellular and Molecular Pharmacology, University of California, San Francisco, San Francisco, CA 94158, USA; Howard Hughes Medical Institute, University of California, San Francisco, San Francisco, CA 94158, USA; California Institute for Quantitative Biomedical Research, San Francisco, CA 94158, USA; Center for RNA Systems Biology, University of California, San Francisco, San Francisco, CA 94158, USA.
Department of Cellular and Molecular Pharmacology, University of California, San Francisco, San Francisco, CA 94158, USA; California Institute for Quantitative Biomedical Research, San Francisco, CA 94158, USA; Center for Systems and Synthetic Biology, University of California, San Francisco, San Francisco, CA 94158, USA.
Cell. 2014 Oct 23;159(3):647-61. doi: 10.1016/j.cell.2014.09.029. Epub 2014 Oct 9.
While the catalog of mammalian transcripts and their expression levels in different cell types and disease states is rapidly expanding, our understanding of transcript function lags behind. We present a robust technology enabling systematic investigation of the cellular consequences of repressing or inducing individual transcripts. We identify rules for specific targeting of transcriptional repressors (CRISPRi), typically achieving 90%-99% knockdown with minimal off-target effects, and activators (CRISPRa) to endogenous genes via endonuclease-deficient Cas9. Together they enable modulation of gene expression over a ∼1,000-fold range. Using these rules, we construct genome-scale CRISPRi and CRISPRa libraries, each of which we validate with two pooled screens. Growth-based screens identify essential genes, tumor suppressors, and regulators of differentiation. Screens for sensitivity to a cholera-diphtheria toxin provide broad insights into the mechanisms of pathogen entry, retrotranslocation and toxicity. Our results establish CRISPRi and CRISPRa as powerful tools that provide rich and complementary information for mapping complex pathways.
尽管哺乳动物转录本及其在不同细胞类型和疾病状态下的表达水平目录正在迅速扩展,但我们对转录本功能的理解仍滞后。我们提出了一种强大的技术,能够系统地研究抑制或诱导单个转录本的细胞后果。我们确定了通过核酸酶缺陷型Cas9对内源基因进行转录抑制因子(CRISPRi)和激活因子(CRISPRa)特异性靶向的规则,通常能实现90%-99%的敲低,脱靶效应最小。它们共同作用可在约1000倍的范围内调节基因表达。利用这些规则,我们构建了全基因组规模的CRISPRi和CRISPRa文库,每个文库都通过两次混合筛选进行了验证。基于生长的筛选确定了必需基因、肿瘤抑制因子和分化调节因子。对霍乱-白喉毒素敏感性的筛选为病原体进入、逆向转运和毒性机制提供了广泛的见解。我们的结果确立了CRISPRi和CRISPRa作为强大工具,为绘制复杂通路提供丰富且互补的信息。