ArticlePloS one2017
Claudin5a is required for proper inflation of Kupffer's vesicle lumen and organ laterality.
Article in PloS one, 2017. 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.
- Natural reversal of cavefish heart asymmetry is controlled by Sonic Hedgehog effects on the left-right organizer.Development (Cambridge, England) · 2024Article
- Understanding laterality disorders and the left-right organizer: Insights from zebrafish.Frontiers in cell and developmental biology · 2022Review
- Simulations of particle tracking in the oligociliated mouse node and implications for left-right symmetry-breaking mechanics.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2020Article
- Akap12beta supports asymmetric heart development via modulating the Kupffer's vesicle formation in zebrafish.BMB reports · 2019Article
- Vertebrate myosin 1d regulates left-right organizer morphogenesis and laterality.Nature communications · 2018Article
- Knockdown of Laminin gamma-3 (Lamc3) impairs motoneuron guidance in the zebrafish embryo.Wellcome open research · 2017Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Left-right asymmetric organ development is critical to establish a proper body plan of vertebrates. In zebrafish, the Kupffer's vesicle (KV) is a fluid-filled sac which controls asymmetric organ development, and a properly inflated KV lumen by means of fluid influx is a prerequisite for the asymmetric signal transmission. However, little is known about the components that support the paracellular tightness between the KV luminal epithelial cells to sustain hydrostatic pressure during KV lumen expansion. Here, we identified that the claudin5a (cldn5a) is highly expressed at the apical surface of KV epithelial cells and tightly seals the KV lumen. Downregulation of cldn5a in zebrafish showed a failure in organ laterality that resulted from malformed KV. In addition, accelerated fluid influx into KV by combined treatment of forskolin and 3-isobutyl-1-methylxanthine failed to expand the partially-formed KV lumen in cldn5a morphants. However, malformed KV lumen and defective heart laterality in cldn5a morphants were significantly rescued by exogenous cldn5a mRNA, suggesting that the tightness between the luminal epithelial cells is important for KV lumen formation. Taken together, these findings suggest that cldn5a is required for KV lumen inflation and left-right asymmetric organ development.
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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.