Evidence map›Paper›PMID 25161212›Full record

ArticleGenetics2014

Efficient marker-free recovery of custom genetic modifications with CRISPR/Cas9 in Caenorhabditis elegans.

Joshua A Arribere, Ryan T Bell, Becky X H Fu, Karen L Artiles, Phil S Hartman, Andrew Z Fire

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 612 papers.

0numbers the graph read from it
0cells of the map it votes in
612citing papers in PubMed
18.2field-weighted citation impact, top 1% 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

612 citing papers in PubMed, 930 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. eIF5A and polyamines restrict mRNA levels in response to ribosome stalls.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  6. Article
  7. Article
  8. Multifaceted and evolutionarily dynamic interactions betweenbioRxiv : the preprint server for biology · 2026
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

552 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

Joshua A ArribereDepartment of Pathology, Stanford University School of Medicine, Stanford, California 94305 arribere@stanford.edu afire@stanford.edu.
Ryan T BellDepartment of Genetics, Stanford University School of Medicine, Stanford, California 94305.
Becky X H FuDepartment of Genetics, Stanford University School of Medicine, Stanford, California 94305.
Karen L ArtilesDepartment of Pathology, Stanford University School of Medicine, Stanford, California 94305.
Phil S HartmanDepartment of Biology, Texas Christian University, Fort Worth, Texas 76129.
Andrew Z FireDepartment of Pathology, Stanford University School of Medicine, Stanford, California 94305 Department of Genetics, Stanford University School of Medicine, Stanford, California 94305 arribere@stanford.edu afire@stanford.edu.
Stanford University · USTexas Christian University · US

Funding

INSTITUTIONAL TRAINING GRANT IN GENOME SCIENCET32HG000044 · NHGRI · STANFORD UNIVERSITY · PI MICHAEL P. SNYDER · 1995 to 2026
$32.2M
GENETICS TRAINING PROGRAM FOR PHD CANDIDATEST32GM007790 · NIGMS · STANFORD UNIVERSITY · PI BRUNET, ANNE, KINGSLEY, DAVID M · 1985 to 2020
$12.8M
GENE REGULATION DURING EARLY DEVELOPMENT OF C. ELEGANSR01GM037706 · NIGMS · STANFORD UNIVERSITY · PI FIRE, ANDREW Z. · 1987 to 2018
$11.0M
Investigating the Ago Cleavage Independent Mechanism(s) of RNAiF32GM112474 · NIGMS · STANFORD UNIVERSITY · PI ARRIBERE, JOSHUA · 2014 to 2017
$141k
NHGRI NIH HHS T32 HG000044NHGRI NIH HHS T32HG000044NIGMS NIH HHS F32 GM112474NIGMS NIH HHS R01 GM037706NIGMS NIH HHS R01GM37706NIGMS NIH HHS T32 GM007790NIGMS NIH HHS T32GM007790
6 · The paper itself

Abstract

Facilitated by recent advances using CRISPR/Cas9, genome editing technologies now permit custom genetic modifications in a wide variety of organisms. Ideally, modified animals could be both efficiently made and easily identified with minimal initial screening and without introducing exogenous sequence at the locus of interest or marker mutations elsewhere. To this end, we describe a coconversion strategy, using CRISPR/Cas9 in which screening for a dominant phenotypic oligonucleotide-templated conversion event at one locus can be used to enrich for custom modifications at another unlinked locus. After the desired mutation is identified among the F1 progeny heterozygous for the dominant marker mutation, F2 animals that have lost the marker mutation are picked to obtain the desired mutation in an unmarked genetic background. We have developed such a coconversion strategy for Caenorhabditis elegans, using a number of dominant phenotypic markers. Examining the coconversion at a second (unselected) locus of interest in the marked F1 animals, we observed that 14-84% of screened animals showed homologous recombination. By reconstituting the unmarked background through segregation of the dominant marker mutation at each step, we show that custom modification events can be carried out recursively, enabling multiple mutant animals to be made. While our initial choice of a coconversion marker [rol-6(su1006)] was readily applicable in a single round of coconversion, the genetic properties of this locus were not optimal in that CRISPR-mediated deletion mutations at the unselected rol-6 locus can render a fraction of coconverted strains recalcitrant to further rounds of similar mutagenesis. An optimal marker in this sense would provide phenotypic distinctions between the desired mutant/+ class and alternative +/+, mutant/null, null/null, and null/+ genotypes. Reviewing dominant alleles from classical C. elegans genetics, we identified one mutation in dpy-10 and one mutation in sqt-1 that meet these criteria and demonstrate that these too can be used as effective conversion markers. Coconversion was observed using a variety of donor molecules at the second (unselected) locus, including oligonucleotides, PCR products, and plasmids. We note that the coconversion approach described here could be applied in any of the variety of systems where suitable coconversion markers can be identified from previous intensive genetic analyses of gain-of-function alleles.

Indexed as

Templates, GeneticAllelesAnimalsBase SequenceCaenorhabditis elegansChromosomesCRISPR-Cas SystemsCrosses, GeneticDNA End-Joining RepairFemaleGene ConversionGenetic LociGenetic MarkersGreen Fluorescent ProteinsHomozygoteMaleGenetic MarkersGreen Fluorescent ProteinsOligonucleotidescoconversionCRISPR/Cas9dpy-10oligonucleotide-mediated homologous recombinationrde-1

Identifiers

PMID25161212
PMCPMC4224173
OpenAlexW2140341433

What OpenQuestion holds

Textmetadata
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.