ArticlePloS one2017
Zebrafish atoh8 mutants do not recapitulate morpholino phenotypes.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 16 papers.
What it found
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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.
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.
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Who cites it
16 citing papers in PubMed, 19 citations in OpenAlex.
- Plag1 Regulates Sensorimotor Modulation in Zebrafish.International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience · 2026Article
- Spatiotemporal control of translation in live zebrafish embryos via photoprotected mRNAs.Communications chemistry · 2025Article
- Bioinformatics Analysis of mRNAs and miRNAs for Identifying Potential Biomarkers in Lung Adenosquamous Carcinoma.Computational and mathematical methods in medicine · 2022Article
- Article
- Targeted deletion of Atoh8 results in severe hearing loss in mice.Genesis (New York, N.Y. : 2000) · 2021Article
- atoh8 expression pattern in early zebrafish embryonic development.Histochemistry and cell biology · 2021Article
- Genotype to Phenotype: CRISPR Gene Editing Reveals Genetic Compensation as a Mechanism for Phenotypic Disjunction of Morphants and Mutants.International journal of molecular sciences · 2021Review
- The ALK-1/SMAD/ATOH8 axis attenuates hypoxic responses and protects against the development of pulmonary arterial hypertension.Science signaling · 2019Article
- An optimised pipeline for parallel image-based quantification of gene expression and genotyping afterBiology open · 2018Article
- Genetic compensation triggered by actin mutation prevents the muscle damage caused by loss of actin protein.PLoS genetics · 2018Article
- Article
- Versatile Genome Engineering Techniques Advance Human Ocular Disease Researches in Zebrafish.Frontiers in cell and developmental biology · 2018Review
- Investigation of Islet2a function in zebrafish embryos: Mutants and morphants differ in morphologic phenotypes and gene expression.PloS one · 2018Article
- Claudin5a is required for proper inflation of Kupffer's vesicle lumen and organ laterality.PloS one · 2017Article
- Knockdown of Laminin gamma-3 (Lamc3) impairs motoneuron guidance in the zebrafish embryo.Wellcome open research · 2017Article
- Article
Corrections and comments
- Erratum issued
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Atoh8 is a bHLH transcription factor expressed in pancreas, skeletal muscle, the nervous system, and cardiovascular tissues during embryological development. Although it has been implicated in the regulation of pancreatic and endothelial cell differentiation, the phenotypic consequences of Atoh8 loss are uncertain. Conclusions from knockout studies in the mouse differ widely depending on the targeting strategy used, while atoh8 knockdown by interfering morpholino oligonucleotides (morpholinos) in zebrafish has led to a range of developmental defects. This study characterised zebrafish embryos homozygous for atoh8sa1465, a loss-of-function allele of atoh8, in order to provide genetic evidence for the developmental role of Atoh8 in this species. Embryos homozygous for atoh8sa1465 present normal body morphology, swimbladder inflation, and heart looping, and survive to adulthood. These embryos do not develop pericardial oedema by 72 hpf and are not sensitised to the loss of Fog1 protein, suggesting that this previously described abnormality is not a specific phenotype. Vascular patterning and primitive haematopoiesis are unaffected in atoh8sa1465/sa1465 mutant embryos. Together, the data suggest that Atoh8 is dispensible for zebrafish development under standard laboratory conditions.
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Registered trials
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.