Evidence map›Paper›PMID 30208061›Full record

ArticlePLoS genetics2018

Robust activation of microhomology-mediated end joining for precision gene editing applications.

Hirotaka Ata, Thomas L Ekstrom, Gabriel Martínez-Gálvez, Carla M Mann, Alexey V Dvornikov, Kyle J Schaefbauer, Alvin C Ma, Drena Dobbs, Karl J Clark, Stephen C Ekker

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
4.2field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

44 citing papers in PubMed, 1 synthesis or guideline pooled it, 81 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 4 institutions in 2 countries.

Hirotaka AtaCenter for Clinical and Translational Science, Mayo Clinic, Rochester, MN, United States of America.
Thomas L EkstromCenter for Clinical and Translational Science, Mayo Clinic, Rochester, MN, United States of America.ORCID 0000-0002-9363-2984
Gabriel Martínez-GálvezGraduate School of Biomedical Sciences, Mayo Clinic, Rochester, MN, United States of America.ORCID 0000-0002-4392-2596
Carla M MannGenetics, Development, and Cell Biology, Iowa State University, Ames, IA, United States of America.
Alexey V DvornikovBiochemistry and Molecular Biology, Mayo Clinic, Rochester, MN, United States of America.ORCID 0000-0003-1514-4747
Kyle J SchaefbauerBiochemistry and Molecular Biology, Mayo Clinic, Rochester, MN, United States of America.
Alvin C MaDepartment of Health Technology and Informatics, The Hong Kong Polytechnic University, Hong Kong, China.
Drena DobbsGenetics, Development, and Cell Biology, Iowa State University, Ames, IA, United States of America.
Karl J ClarkBiochemistry and Molecular Biology, Mayo Clinic, Rochester, MN, United States of America.ORCID 0000-0002-9637-0967
Stephen C EkkerCenter for Clinical and Translational Science, Mayo Clinic, Rochester, MN, United States of America.ORCID 0000-0003-0726-4212
Mayo Clinic in Florida · USMayo Clinic · USIowa State University · USHong Kong Polytechnic University · HK

Funding

Mayo Clinic Center for Clinical and Translational Science (CCaTS UL1 Supplement - Dr. Timothy Curry)UL1TR002377 · NCATS · MAYO CLINIC ROCHESTER · PI VESNA D GAROVIC · 2017 to 2026
$78.4M
PILOT AND FEASIBILTY PROGRAMP30DK084567 · NIDDK · MAYO CLINIC ROCHESTER · PI GREGORY J. GORES · 2009 to 2026
$22.2M
Pilot and FeasibilityP30DK090728 · NIDDK · MAYO CLINIC ROCHESTER · PI ROMERO, MICHAEL F. · 2010 to 2019
$11.8M
Systematic Vertebrate Functional GenomicsR01GM063904 · NIGMS · UNIVERSITY OF TEXAS AT AUSTIN · PI EKKER, STEPHEN CARL · 2001 to 2025
$10.7M
In vivo model of microglia inflammasome signaling in neuroinflammationR24OD020166 · OD · IOWA STATE UNIVERSITY · PI CLARK, KARL J, EKKER, STEPHEN CARL · 2016 to 2023
$7.1M
Medical Scientist Traning Program at Mayo ClinicT32GM065841 · NIGMS · MAYO CLINIC ROCHESTER · PI KAUFMANN, SCOTT H, SCHIMMENTI, LISA A · 2003 to 2022
$5.8M
Systematic Vertebrate Functional GenomicsR56GM063904 · NIGMS · MAYO CLINIC ROCHESTER · PI EKKER, STEPHEN CARL · 2009 to 2010
$611k
American Heart Association-American Stroke Association 16PRE30470004NCATS NIH HHS UL1 TR002377NIDDK NIH HHS P30 DK084567NIDDK NIH HHS P30 DK090728NIGMS NIH HHS R01 GM063904NIGMS NIH HHS R56 GM063904NIGMS NIH HHS T32 GM065841NIH HHS R24 OD020166
6 · The paper itself

Abstract

One key problem in precision genome editing is the unpredictable plurality of sequence outcomes at the site of targeted DNA double stranded breaks (DSBs). This is due to the typical activation of the versatile Non-homologous End Joining (NHEJ) pathway. Such unpredictability limits the utility of somatic gene editing for applications including gene therapy and functional genomics. For germline editing work, the accurate reproduction of the identical alleles using NHEJ is a labor intensive process. In this study, we propose Microhomology-mediated End Joining (MMEJ) as a viable solution for improving somatic sequence homogeneity in vivo, capable of generating a single predictable allele at high rates (56% ~ 86% of the entire mutant allele pool). Using a combined dataset from zebrafish (Danio rerio) in vivo and human HeLa cell in vitro, we identified specific contextual sequence determinants surrounding genomic DSBs for robust MMEJ pathway activation. We then applied our observation to prospectively design MMEJ-inducing sgRNAs against a variety of proof-of-principle genes and demonstrated high levels of mutant allele homogeneity. MMEJ-based DNA repair at these target loci successfully generated F0 mutant zebrafish embryos and larvae that faithfully recapitulated previously reported, recessive, loss-of-function phenotypes. We also tested the generalizability of our approach in cultured human cells. Finally, we provide a novel algorithm, MENTHU (http://genesculpt.org/menthu/), for improved and facile prediction of candidate MMEJ loci. We believe that this MMEJ-centric approach will have a broader impact on genome engineering and its applications. For example, whereas somatic mosaicism hinders efficient recreation of knockout mutant allele at base pair resolution via the standard NHEJ-based approach, we demonstrate that F0 founders transmitted the identical MMEJ allele of interest at high rates. Most importantly, the ability to directly dictate the reading frame of an endogenous target will have important implications for gene therapy applications in human genetic diseases.

Indexed as

DNA Breaks, Double-StrandedModels, GeneticAlgorithmsAllelesAnimalsDNA End-Joining RepairFeasibility StudiesFemaleGene EditingGenetic Diseases, InbornGenetic TherapyHeLa CellsHumansMaleMutagenesis, Site-DirectedRNA, Guide, CRISPR-Cas SystemsRNA, Guide, CRISPR-Cas Systems

Identifiers

PMID30208061
PMCPMC6152997
OpenAlexW2889830609

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.