ArticleDevelopmental biology2012
Mutation of zebrafish Snapc4 is associated with loss of the intrahepatic biliary network.
Article in Developmental biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed, 21 citations in OpenAlex.
- Forward genetics combined with unsupervised classifications identified zebrafish mutants affecting biliary system formation.Developmental biology · 2024Article
- Zebrafish as a Model for Cardiovascular and Metabolic Disease: The Future of Precision Medicine.Biomedicines · 2024Review
- Review
- Bi-allelic SNAPC4 variants dysregulate global alternative splicing and lead to neuroregression and progressive spastic paraparesis.American journal of human genetics · 2023Article
- NCK-associated protein 1 like (nckap1l) minor splice variant regulates intrahepatic biliary network morphogenesis.PLoS genetics · 2021Article
- Three-dimensional structural analysis reveals a Cdk5-mediated kinase cascade regulating hepatic biliary network branching in zebrafish.Development (Cambridge, England) · 2017Article
- LITTLE FISH, BIG DATA: ZEBRAFISH AS A MODEL FOR CARDIOVASCULAR AND METABOLIC DISEASE.Physiological reviews · 2017Review
- Making It New Again: Insight Into Liver Development, Regeneration, and Disease From Zebrafish Research.Current topics in developmental biology · 2017Review
- Zebrafish: an important tool for liver disease research.Gastroenterology · 2015Review
- The lure of zebrafish in liver research: regulation of hepatic growth in development and regeneration.Current opinion in genetics & development · 2015Review
- Homeostatic generation of reactive oxygen species protects the zebrafish liver from steatosis.Hepatology (Baltimore, Md.) · 2013Article
- Zebrafish models of human liver development and disease.Comprehensive Physiology · 2013Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Biliary epithelial cells line the intrahepatic biliary network, a complex three-dimensional network of conduits. The loss of differentiated biliary epithelial cells is the primary cause of many congenital liver diseases. We identified a zebrafish snapc4 (small nuclear RNA-activating complex polypeptide 4) mutant in which biliary epithelial cells initially differentiate but subsequently disappear. In these snapc4 mutant larvae, biliary epithelial cells undergo apoptosis, leading to degeneration of the intrahepatic biliary network. Consequently, in snapc4 mutant larvae, biliary transport of ingested fluorescent lipids to the gallbladder is blocked. Snapc4 is the largest subunit of a protein complex that regulates small nuclear RNA (snRNA) transcription. The snapc4(s445) mutation causes a truncation of the C-terminus, thereby deleting the domain responsible for a specific interaction with Snapc2, a vertebrate specific subunit of the SNAP complex. This mutation leads to a hypomorphic phenotype, as only a subset of snRNA transcripts are quantitatively altered in snapc4(s445) mutant larvae. snapc2 knockdown also disrupts the intrahepatic biliary network in a similar fashion as in snapc4(s445) mutant larvae. These data indicate that the physical interaction between Snapc2 and Snapc4 is important for the expression of a subset of snRNAs and biliary epithelial cell survival in zebrafish.
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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.