Evidence map›Paper›PMID 25685662›Full record

ArticleFEBS open bio2015

Creation of targeted genomic deletions using TALEN or CRISPR/Cas nuclease pairs in one-cell mouse embryos.

Christina Brandl, Oskar Ortiz, Bernhard Röttig, Benedikt Wefers, Wolfgang Wurst, Ralf Kühn

Open access · goldAbstract read
In one paragraph

Article in FEBS open bio, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

24 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Recent Advances in the Production of Genome-Edited Rats.International journal of molecular sciences · 2022
    Review
  3. Article
  4. Review
  5. Article
  6. Efficient mutagenesis targeting theAmerican journal of translational research · 2021
    Article
  7. Article
  8. GPRIN3 Controls Neuronal Excitability, Morphology, and Striatal-Dependent Behaviors in the Indirect Pathway of the Striatum.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  9. Article
  10. Article
  11. The Application of CRISPR/Cas9 for the Treatment of Retinal Diseases.The Yale journal of biology and medicine · 2017
    Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. CRISPR/Cas9-Mediated Genome Editing as a Therapeutic Approach for Leber Congenital Amaurosis 10.Molecular therapy : the journal of the American Society of Gene Therapy · 2017
    Article
  17. Article
  18. Review
  19. Article
  20. Article
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

6 authors at 3 institutions in 1 country.

Christina BrandlInstitute of Developmental Genetics, Helmholtz Zentrum München, German Research Center for Environmental Health, 85764 Neuherberg, Germany ; Technische Universität München, 85350 Freising-Weihenstephan, Germany.
Oskar OrtizInstitute of Developmental Genetics, Helmholtz Zentrum München, German Research Center for Environmental Health, 85764 Neuherberg, Germany.
Bernhard RöttigInstitute of Developmental Genetics, Helmholtz Zentrum München, German Research Center for Environmental Health, 85764 Neuherberg, Germany ; Technische Universität München, 85350 Freising-Weihenstephan, Germany.
Benedikt WefersInstitute of Developmental Genetics, Helmholtz Zentrum München, German Research Center for Environmental Health, 85764 Neuherberg, Germany ; Deutsches Zentrum für Neurodegenerative Erkrankungen e.V. (DZNE), 80336 Munich, Germany.
Wolfgang WurstInstitute of Developmental Genetics, Helmholtz Zentrum München, German Research Center for Environmental Health, 85764 Neuherberg, Germany ; Technische Universität München, 85350 Freising-Weihenstephan, Germany ; Deutsches Zentrum für Neurodegenerative Erkrankungen e.V. (DZNE), 80336 Munich, Germany ; Max-Planck-Institute of Psychiatry, 80804 Munich, Germany ; Munich Cluster for Systems Neurology (SyNergy), Ludwig-Maximilians-Universität München, 80336 Munich, Germany.
Ralf KühnInstitute of Developmental Genetics, Helmholtz Zentrum München, German Research Center for Environmental Health, 85764 Neuherberg, Germany ; Technische Universität München, 85350 Freising-Weihenstephan, Germany ; Max-Delbrück-Centrum für Molekulare Medizin (MDC), 13125 Berlin, Germany.
Helmholtz Zentrum München · DETechnical University of Munich · DEGerman Center for Neurodegenerative Diseases · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The use of TALEN and CRISPR/CAS nucleases is becoming increasingly popular as a means to edit single target sites in one-cell mouse embryos. Nevertheless, an area that has received less attention concerns the engineering of structural genome variants and the necessary religation of two distant double-strand breaks. Herein, we applied pairs of TALEN or sgRNAs and Cas9 to create deletions in the Rab38 gene. We found that the deletion of 3.2 or 9.3 kb, but not of 30 kb, occurs at a frequency of 6-37%. This is sufficient for the direct production of mutants by embryo microinjection. Therefore, deletions up to ∼10 kb can be readily achieved for modeling human disease alleles. This work represents an important step towards the establishment of new protocols that support the ligation of remote DSB ends to achieve even larger rearrangements.

Indexed as

Cas9CRISPRDisease modelDSB, double-strand breakES, embryonic stem (cell)HR, homologous recombinationMouse mutantNHEJ, non-homologous end joiningOne-cell embryosg, single guideTALENsTALEN, TAL effector nucleasesTAL, transcription activator-likeZFN, zinc-finger nucleases

Identifiers

PMID25685662
PMCPMC4309836
OpenAlexW1997997850

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.