Evidence map›Paper›PMID 32112658›Full record

ArticleJournal of fish biology2021

Transgene-mediated skeletal phenotypic variation in zebrafish.

Charles B Kimmel, Alexander L Wind, Whitney Oliva, Samuel D Ahlquist, Charline Walker, John Dowd, Bernardo Blanco-Sánchez, Tom A Titus, Peter Batzel, Jared C Talbot and 2 more

Open access · greenAbstract read
In one paragraph

Article in Journal of fish biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.9field-weighted citation impact, top 24% 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

7 citing papers in PubMed, 10 citations in OpenAlex.

  1. Early ultraviolet exposure disrupts late dorsal fin skeletal development in zebrafish.Developmental dynamics : an official publication of the American Association of Anatomists · 2026
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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

12 authors at 3 institutions in 1 country.

Charles B KimmelInstitute of Neuroscience, University of Oregon, Eugene, Oregon, USA.ORCID https://orcid.org/0000-0002-1122-4371
Alexander L WindInstitute of Neuroscience, University of Oregon, Eugene, Oregon, USA.
Whitney OlivaInstitute of Neuroscience, University of Oregon, Eugene, Oregon, USA.
Samuel D AhlquistInstitute of Neuroscience, University of Oregon, Eugene, Oregon, USA.
Charline WalkerInstitute of Neuroscience, University of Oregon, Eugene, Oregon, USA.
John DowdInstitute of Neuroscience, University of Oregon, Eugene, Oregon, USA.
Bernardo Blanco-SánchezInstitute of Neuroscience, University of Oregon, Eugene, Oregon, USA.
Tom A TitusInstitute of Neuroscience, University of Oregon, Eugene, Oregon, USA.
Peter BatzelInstitute of Neuroscience, University of Oregon, Eugene, Oregon, USA.
Jared C TalbotSchool of Biology and Ecology, University of Maine, Orono, Maine, USA.ORCID https://orcid.org/0000-0001-8941-6325
John H PostlethwaitInstitute of Neuroscience, University of Oregon, Eugene, Oregon, USA.ORCID https://orcid.org/0000-0002-5476-2137
James T NicholsDepartment of Craniofacial Biology, University of Colorado Anschutz Medical Campus, Aurora, Colorado, USA.ORCID https://orcid.org/0000-0002-7263-1704
University of Oregon · USUniversity of Colorado Anschutz Medical Campus · USUniversity of Maine · US

Funding

Zebrafish FacilityP01HD022486 · NICHD · UNIVERSITY OF OREGON · PI PARTHASARATHY, RAGHUVEER · 1987 to 2017
$28.8M
CRANIOFACIAL MORPHOGENESIS IN ZEBRAFISHR01DE013834 · NIDCR · UNIVERSITY OF OREGON · PI KIMMEL, CHARLES B · 2000 to 2014
$6.9M
DEVELOPMENTAL BIOLOGY TRAINING PROGRAMT32HD007348 · NICHD · UNIVERSITY OF OREGON · PI Chris Q Doe, KRYN STANKUNAS · 1989 to 2026
$6.8M
Resources for Teleost Gene Duplicates and Human DiseaseR01OD011116 · OD · UNIVERSITY OF OREGON · PI POSTLETHWAIT, JOHN H. · 2012 to 2020
$5.4M
NICHD R25 Summer Research Program at the University of OregonR25HD070817 · NICHD · UNIVERSITY OF OREGON · PI EISEN, JUDITH S · 2011 to 2021
$1.1M
Cell Fate Choices in the SkeletonR00DE024190 · NIDCR · UNIVERSITY OF COLORADO DENVER · PI NICHOLS, JAMES TUCKER · 2017 to 2019
$887k
NICHD NIH HHS P01 HD022486NICHD NIH HHS P01-HD022486NICHD NIH HHS R25 HD070817NICHD NIH HHS T32 HD007348NIDCR NIH HHS R00 DE024190NIDCR NIH HHS R00-DE024190NIDCR NIH HHS R01 DE013834NIDCR NIH HHS R01-DE13834NIH HHS NICHD P01-HD022486NIH HHS NICHD P01-HD022486.NIH HHS NIDCR R01-DE13834NIH HHS R00-DE024190NIH HHS R01 OD011116
6 · The paper itself

Abstract

When considering relationships between genotype and phenotype we frequently ignore the fact that the genome of a typical animal, notably including that of a fish and a human, harbours a huge amount of foreign DNA. Such DNA, in the form of transposable elements, can affect genome function in a major way, and transgene biology needs to be included in our understanding of the genome. Here we examine an unexpected phenotypic effect of the chromosomally integrated transgene fli1a-F-hsp70l:Gal4VP16 that serves as a model for transgene function generally. We examine larval fras1 mutant zebrafish (Danio rerio). Gal4VP16 is a potent transcriptional activator that is already well known for toxicity and mediating unusual transcriptional effects. In the presence of the transgene, phenotypes in the neural crest-derived craniofacial skeleton, notably fusions and shape changes associated with loss of function fras1 mutations, are made more severe, as we quantify by scoring phenotypic penetrance, the fraction of mutants expressing the trait. A very interesting feature is that the enhancements are highly specific for fras1 mutant phenotypes, occurring in the apparent absence of more widespread changes. Except for the features due to the fras1 mutation, the transgene-bearing larvae appear generally healthy and to be developing normally. The transgene behaves as a genetic partial dominant: a single copy is sufficient for the enhancements, yet, for some traits, two copies may exert a stronger effect. We made new strains bearing independent insertions of the fli1a-F-hsp70l:Gal4VP16 transgene in new locations in the genome, and observed increased severities of the same phenotypes as observed for the original insertion. This finding suggests that sequences within the transgene, for example Gal4VP16, are responsible for the enhancements, rather than the effect on neighbouring host sequences (such as an insertional mutation). The specificity and biological action underlying the traits are subjects of considerable interest for further investigation, as we discuss. Our findings show that work with transgenes needs to be undertaken with caution and attention to detail.

Indexed as

Biological Variation, PopulationAnimalsBone and BonesBone DevelopmentHumansMutationPhenotypeTransgenesZebrafishcanalizationcraniofacial skeletonfras1Fraser syndromeGal4VP16opercleskeletal fusion

Identifiers

PMID32112658
PMCPMC7483860
OpenAlexW3007130829

What OpenQuestion holds

Textmetadata
LicenceTDM
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.