Evidence map›Paper›PMID 32054870›Full record

ArticleScientific reports2020

Enhanced homologous recombination by the modulation of targeting vector ends.

Shinji Hirotsune, Hiroshi Kiyonari, Mingyue Jin, Kanako Kumamoto, Kayo Yoshida, Miki Shinohara, Hitomi Watanabe, Anthony Wynshaw-Boris, Fumio Matsuzaki

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.8field-weighted citation impact, top 31% 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

8 citing papers in PubMed, 11 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

9 authors at 4 institutions in 2 countries.

Shinji HirotsuneDepartment of Genetic Disease Research, Osaka City University, Graduate School of Medicine, Asahi-machi 1-4-3, Abeno, Osaka, 545-8585, Japan. shinjih@med.osaka-cu.ac.jp.
Hiroshi KiyonariAnimal Resource Development Unit, Genetic Engineering Team, Division of Bio-Function Dynamics Imaging, RIKEN Center for Life Science Technologies, 2-2-3 Minatojima-Minamimachi, Chuou-ku, Kobe, 650-0047, Japan.
Mingyue JinDepartment of Genetic Disease Research, Osaka City University, Graduate School of Medicine, Asahi-machi 1-4-3, Abeno, Osaka, 545-8585, Japan.ORCID http://orcid.org/0000-0002-5249-8918
Kanako KumamotoDepartment of Genetic Disease Research, Osaka City University, Graduate School of Medicine, Asahi-machi 1-4-3, Abeno, Osaka, 545-8585, Japan.
Kayo YoshidaLaboratory Animal Science, Osaka City University, Graduate School of Medicine, Asahi-machi 1-4-3, Abeno, Osaka, 545-8585, Japan.
Miki ShinoharaInstitute for Protein Research, Osaka University 3-2 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Hitomi WatanabeLaboratory of Integrative Biological Science, Institute for Frontier Life and Medical Sciences, Kyoto University, Kyoto, 606-8507, Japan.
Anthony Wynshaw-BorisDepartment of Genetics and Genome Sciences, Case Western Reserve University, School of Medicine, University Hospitals Case Medical Center 10900 Euclid Avenue, BRB731, Cleveland, Ohio, 44106-4955, USA.
Fumio MatsuzakiRIKEN Center for Developmental Biology, 2-2-3 Minatojima-Minamimachi, Chuou-ku, Kobe, 650-0047, Japan.ORCID http://orcid.org/0000-0001-7902-4520
Osaka City University · JPKyoto University · JPProtein Research Foundation · JPUniversity Hospitals Cleveland Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The field of genome editing was founded on the establishment of methods, such as the clustered regularly interspaced short palindromic repeat (CRISPR) and CRISPR-associated protein (CRISPR/Cas) system, used to target DNA double-strand breaks (DSBs). However, the efficiency of genome editing also largely depends on the endogenous cellular repair machinery. Here, we report that the specific modulation of targeting vectors to provide 3' overhangs at both ends increased the efficiency of homology-directed repair (HDR) in embryonic stem cells. We applied the modulated targeting vectors to produce homologous recombinant mice directly by pronuclear injection, but the frequency of HDR was low. Furthermore, we combined our method with the CRISPR/Cas9 system, resulting in a significant increase in HDR frequency. Thus, our HDR-based method, enhanced homologous recombination for genome targeting (eHOT), is a new and powerful method for genome engineering.

Indexed as

CRISPR-Cas SystemsDNA Breaks, Double-StrandedGene EditingGene TargetingHomologous RecombinationAnimalsClustered Regularly Interspaced Short Palindromic RepeatsFemaleGenetic VectorsMiceMice, Inbred C57BLMice, Inbred ICRRecombinational DNA Repair

Identifiers

PMID32054870
PMCPMC7018964
OpenAlexW3006352510

What OpenQuestion holds

Textmetadata
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.