MAGeCK enables robust identification of essential genes from genome-scale CRISPR/Cas9 knockout screens

We propose the Model-based Analysis of Genome-wide CRISPR/Cas9 Knockout (MAGeCK) method for prioritizing single-guide RNAs, genes and pathways in genome-scale CRISPR/Cas9 knockout screens. MAGeCK demonstrates better performance compared with existing methods, identifies both positively and negativel...

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Bibliographic Details
Published in:Genome biology Vol. 15; no. 12; p. 554
Main Authors: Li, Wei, Xu, Han, Xiao, Tengfei, Cong, Le, Love, Michael I, Zhang, Feng, Irizarry, Rafael A, Liu, Jun S, Brown, Myles, Liu, X Shirley
Format: Journal Article
Language:English
Published: London BioMed Central 05.12.2014
Subjects:
Algorithms
Animal Genetics and Genomics
Bioinformatics
Biomedical and Life Sciences
Cell Line, Tumor
Computational Biology - methods
CRISPR-Associated Proteins - genetics
CRISPR-Cas Systems
data collection
essential genes
Evolutionary Biology
Gene Expression Regulation, Neoplastic
Gene Knockout Techniques
Genes, Essential
Genetic Predisposition to Disease
HL-60 Cells
Human Genetics
Humans
insulin
Life Sciences
Method
Microbial Genetics and Genomics
mutation
Neoplasms - genetics
Plant Genetics and Genomics
RNA
signal transduction
False Discovery Rate
Sequencing Depth
Read Count
Essential Gene
Negative Binomial Distribution
ISSN:1474-760X, 1465-6906, 1474-760X, 1465-6914
Online Access:Get full text
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Summary:We propose the Model-based Analysis of Genome-wide CRISPR/Cas9 Knockout (MAGeCK) method for prioritizing single-guide RNAs, genes and pathways in genome-scale CRISPR/Cas9 knockout screens. MAGeCK demonstrates better performance compared with existing methods, identifies both positively and negatively selected genes simultaneously, and reports robust results across different experimental conditions. Using public datasets, MAGeCK identified novel essential genes and pathways, including EGFR in vemurafenib-treated A375 cells harboring a BRAF mutation. MAGeCK also detected cell type-specific essential genes, including BCR and ABL1 , in KBM7 cells bearing a BCR-ABL fusion, and IGF1R in HL-60 cells, which depends on the insulin signaling pathway for proliferation.
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ISSN:1474-760X
1465-6906
1474-760X
1465-6914
DOI:10.1186/s13059-014-0554-4