Evidence map›Paper›PMID 28005909›Full record

ArticlePloS one2016

Neural Crest Migration and Survival Are Susceptible to Morpholino-Induced Artifacts.

Elena F Boer, Cicely A Jette, Rodney A Stewart

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. 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
2.4field-weighted citation impact, top 11% 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, 20 citations in OpenAlex.

  1. Disruption ofFrontiers in cell and developmental biology · 2023
    Article
  2. Frontiers in cell and developmental biology · 2022
    Article
  3. Review
  4. PeerJ · 2019
    Article
  5. Article
  6. Article
  7. Article
  8. 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

3 authors at 1 institution in 1 country.

Elena F BoerDepartment of Oncological Sciences, Huntsman Cancer Institute, University of Utah, Salt Lake City, Utah, United States of America.ORCID http://orcid.org/0000-0002-7015-4852
Cicely A JetteDepartment of Oncological Sciences, Huntsman Cancer Institute, University of Utah, Salt Lake City, Utah, United States of America.
Rodney A StewartDepartment of Oncological Sciences, Huntsman Cancer Institute, University of Utah, Salt Lake City, Utah, United States of America.ORCID http://orcid.org/0000-0003-1220-1830
University of Utah · US

Funding

DEVELOPMENTAL BIOLOGY TRAINING PROGRAMT32HD007491 · NICHD · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI James Alan Gagnon, Kristen M Kwan · 1995 to 2026
$8.0M
NCRR Confocal ProposalS10RR024761 · NCRR · UNIVERSITY OF UTAH · PI RODESCH, CHRISTOPHER K · 2008 to 2008
$475k
HSRD VA CDA 13-025NCRR NIH HHS S10 RR024761NICHD NIH HHS T32 HD007491
6 · The paper itself

Abstract

The neural crest (NC) is a stem cell-like embryonic population that is essential for generating and patterning the vertebrate body, including the craniofacial skeleton and peripheral nervous system. Defects in NC development underlie many birth defects and contribute to formation of some of the most malignant cancers in humans, such as melanoma and neuroblastoma. For these reasons, significant research efforts have been expended to identify genes that control NC development, as it is expected to lead to a deeper understanding of the genetic mechanisms controlling vertebrate development and identify new treatments for NC-derived diseases and cancers. However, a number of inconsistencies regarding gene function during NC development have emerged from comparative analyses of gene function between mammalian and non-mammalian systems (chick, frog, zebrafish). This poses a significant barrier to identification of single genes and/or redundant pathways to target in NC diseases. Here, we determine whether technical differences, namely morpholino-based approaches used in non-mammalian systems, could contribute to these discrepancies, by examining the extent to which NC phenotypes in fascin1a (fscn1a) morphant embryos are similar to or different from fscn1a null mutants in zebrafish. Analysis of fscn1a morphants showed that they mimicked early NC phenotypes observed in fscn1a null mutants; however, these embryos also displayed NC migration and derivative phenotypes not observed in null mutants, including accumulation of p53-independent cell death. These data demonstrate that morpholinos can cause seemingly specific NC migration and derivative phenotypes, and thus have likely contributed to the inconsistencies surrounding NC gene function between species. We suggest that comparison of genetic mutants between different species is the most rigorous method for identifying conserved genetic mechanisms controlling NC development and is critical to identify new treatments for NC diseases.

Indexed as

AnimalsAnimals, Genetically ModifiedApoptosisBody PatterningCell MovementEmbryo, NonmammalianIn Situ Hybridization, FluorescenceMicrofilament ProteinsMicroscopy, ConfocalMorpholinosNeural CrestPhenotypePseudopodiaRNA, MessengerTumor Suppressor Protein p53Zebrafishfscn1a protein, zebrafishMicrofilament ProteinsMorpholinosRNA, MessengerTumor Suppressor Protein p53Zebrafish Proteins

Identifiers

PMID28005909
PMCPMC5179070
OpenAlexW2570307402

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.