Evidence map›Paper›PMID 38768228›Full record

ArticlePLoS computational biology2024

A dose-response model for statistical analysis of chemical genetic interactions in CRISPRi screens.

Sanjeevani Choudhery, Michael A DeJesus, Aarthi Srinivasan, Jeremy Rock, Dirk Schnappinger, Thomas R Ioerger

Abstract read
In one paragraph

Article in PLoS computational biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors.

Sanjeevani ChoudheryDepartment of Computer Science and Engineering, Texas A&M University, College Station, Texas, United States of America.ORCID 0009-0008-4101-4712
Michael A DeJesusLaboratory of Host-Pathogen Biology, The Rockefeller University, New York, New York, United States of America.ORCID 0000-0003-3867-0299
Aarthi SrinivasanDepartment of Computer Science and Engineering, Texas A&M University, College Station, Texas, United States of America.
Jeremy RockLaboratory of Host-Pathogen Biology, The Rockefeller University, New York, New York, United States of America.
Dirk SchnappingerDepartment of Microbiology and Immunology, Weill Cornell Medical College, New York, New York, United States of America.
Thomas R IoergerDepartment of Computer Science and Engineering, Texas A&M University, College Station, Texas, United States of America.

Funding

Surviving evolution: Short-term adaptations for fitnessP01AI143575 · NIAID · WEILL MEDICAL COLL OF CORNELL UNIV · PI SABINE EHRT · 2020 to 2026
$18.2M
NIAID NIH HHS P01 AI143575
6 · The paper itself

Abstract

An important application of CRISPR interference (CRISPRi) technology is for identifying chemical-genetic interactions (CGIs). Discovery of genes that interact with exposure to antibiotics can yield insights to drug targets and mechanisms of action or resistance. The objective is to identify CRISPRi mutants whose relative abundance is suppressed (or enriched) in the presence of a drug when the target protein is depleted, reflecting synergistic behavior. Different sgRNAs for a given target can induce a wide range of protein depletion and differential effects on growth rate. The effect of sgRNA strength can be partially predicted based on sequence features. However, the actual growth phenotype depends on the sensitivity of cells to depletion of the target protein. For essential genes, sgRNA efficiency can be empirically measured by quantifying effects on growth rate. We observe that the most efficient sgRNAs are not always optimal for detecting synergies with drugs. sgRNA efficiency interacts in a non-linear way with drug sensitivity, producing an effect where the concentration-dependence is maximized for sgRNAs of intermediate strength (and less so for sgRNAs that induce too much or too little target depletion). To capture this interaction, we propose a novel statistical method called CRISPRi-DR (for Dose-Response model) that incorporates both sgRNA efficiencies and drug concentrations in a modified dose-response equation. We use CRISPRi-DR to re-analyze data from a recent CGI experiment in Mycobacterium tuberculosis to identify genes that interact with antibiotics. This approach can be generalized to non-CGI datasets, which we show via an CRISPRi dataset for E. coli growth on different carbon sources. The performance is competitive with the best of several related analytical methods. However, for noisier datasets, some of these methods generate far more significant interactions, likely including many false positives, whereas CRISPRi-DR maintains higher precision, which we observed in both empirical and simulated data.

Indexed as

Anti-Bacterial AgentsClustered Regularly Interspaced Short Palindromic RepeatsComputational BiologyCRISPR-Cas SystemsDose-Response Relationship, DrugEscherichia coliModels, GeneticModels, StatisticalMycobacterium tuberculosisRNA, Guide, CRISPR-Cas SystemsAnti-Bacterial AgentsRNA, Guide, CRISPR-Cas Systems

Identifiers

PMID38768228
PMCPMC11104602

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LicenceCC BY
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.