Evidence map›Paper›PMID 30210230›Full record

ArticleMolecular vision2018

Targeted disruption of the endogenous zebrafish

Christopher P Zelinka, Mailin Sotolongo-Lopez, James M Fadool

Open access · greenAbstract read
In one paragraph

Article in Molecular vision, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

14 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Article
  3. An Overview towards Zebrafish Larvae as a Model for Ocular Diseases.International journal of molecular sciences · 2023
    Review
  4. Retinal Cone Mosaic in sws1-Mutant Medaka (Oryzias latipes), A Teleost.Investigative ophthalmology & visual science · 2022
    Article
  5. Review
  6. Article
  7. Article
  8. Zebrafish models of inherited retinal dystrophies.Journal of translational genetics and genomics · 2022
    Article
  9. Biochemistry and physiology of zebrafish photoreceptors.Pflugers Archiv : European journal of physiology · 2021
    Review
  10. Review
  11. Review
  12. Loss of Pde6a Induces Rod Outer Segment Shrinkage and Visual Alterations inFrontiers in cell and developmental biology · 2021
    Article
  13. Review
  14. Review
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

3 authors at 1 institution in 1 country.

Christopher P ZelinkaDepartment of Biological Science, Florida State University, Tallahassee, FL.
Mailin Sotolongo-LopezDepartment of Biological Science, Florida State University, Tallahassee, FL.
James M FadoolDepartment of Biological Science, Florida State University, Tallahassee, FL.
Florida State University · US

Funding

Disease Models for High Throughput ScreensR21EY025410 · NEI · FLORIDA STATE UNIVERSITY · PI FADOOL, JAMES M · 2015 to 2016
$393k
NEI NIH HHS R21 EY025410
6 · The paper itself

Abstract

Purpose: Retinitis pigmentosa (RP) is a collection of genetic disorders that results in the degeneration of light-sensitive photoreceptor cells, leading to blindness. RP is associated with more than 70 loci that may display dominant or recessive modes of inheritance, but mutations in the gene encoding the visual pigment rhodopsin (RHO) are the most frequent cause. In an effort to develop precise mutations in zebrafish as novel models of photoreceptor degeneration, we describe the generation and germline transmission of a series of novel clustered regularly interspaced short palindromic repeats (CRISPR)/Cas9-induced insertion and deletion (indel) mutations in the major zebrafish Methods: One- or two-cell staged zebrafish embryos were microinjected with in vitro transcribed mRNA encoding Cas9 and a single guide RNA (gRNA). Mutations were detected by restriction fragment length polymorphism (RFLP) and DNA sequence analyses in injected embryos and offspring. Immunolabeling with rod- and cone-specific antibodies was used to test for histological and cellular changes. Results: Using gRNAs that targeted highly conserved regions of Conclusions: The efficiency of CRISPR/Cas9 for gene targeting, coupled with the large number of mutations associated with RP, provided a backdrop for the rapid isolation of novel alleles in zebrafish that phenocopy disease. These novel lines will provide much needed in-vivo models for high throughput screens of compounds or genes that protect from photoreceptor degeneration.

Indexed as

Disease Models, AnimalAnimalsAnimals, Genetically ModifiedCodon, TerminatorCRISPR-Cas SystemsFrameshift MutationGene TargetingImmunoblottingPolymorphism, Restriction Fragment LengthRetinal DegenerationRetinal Rod Photoreceptor CellsRhodopsinRNA, MessengerZebrafishZebrafish ProteinsCodon, TerminatorRhodopsinRNA, MessengerZebrafish Proteins

Identifiers

PMID30210230
PMCPMC6128699
OpenAlexW2985033178

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.