ArticleDevelopmental dynamics : an official publication of the American Association of Anatomists2013
Zebrafish churchill regulates developmental gene expression and cell migration.
Article in Developmental dynamics : an official publication of the American Association of Anatomists, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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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.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Analysis of multiple gene co-expression networks to discover interactions favoring CFTR biogenesis and ΔF508-CFTR rescue.BMC medical genomics · 2021Article
- Reduction in Toxicity of Nano-Ag-Polyvinyl-pyrrolidone UsingNanomaterials (Basel, Switzerland) · 2019Article
- Editing of the Luteinizing Hormone Gene to Sterilize Channel Catfish, Ictalurus punctatus, Using a Modified Zinc Finger Nuclease Technology with Electroporation.Marine biotechnology (New York, N.Y.) · 2016Article
- Article
- Mutagenesis and phenotyping resources in zebrafish for studying development and human disease.Briefings in functional genomics · 2014Review
- Chromosomal deletions and inversions mediated by TALENs and CRISPR/Cas in zebrafish.Nucleic acids research · 2013Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
backgroundRegulation of developmental signaling pathways is essential for embryogenesis. The small putative zinc finger protein, Churchill (ChCh) has been implicated in modulation of both TGF-β and FGF signaling.
resultsWe used zinc finger nuclease (ZFN) mediated gene targeting to disrupt the zebrafish chch locus and generate the first chch mutations. Three induced lesions produce frameshift mutations that truncate the protein in the third of five β-strands that comprise the protein. Surprisingly, zygotic and maternal zygotic chch mutants are viable. Mutants have elevated expression of mesodermal markers, but progress normally through early development. chch mutants are sensitive to exogenous Nodal. However, neither misregulation of FGF targets nor sensitivity to exogenous FGF was detected. Finally, chch mutant cells were found to undergo inappropriate migration in cell transplant assays.
conclusionsTogether, these results suggest that chch is not essential for survival, but functions to modulate early mesendodermal gene expression and limit cell migration.
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Registered trials
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