ArticleDevelopmental biology2012
An essential and highly conserved role for Zic3 in left-right patterning, gastrulation and convergent extension morphogenesis.
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 23 papers.
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.
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.
Who cites it
23 citing papers in PubMed, 33 citations in OpenAlex.
- Broadening horizons: new links between cilia and heart development and disease.Frontiers in cardiovascular medicine · 2026Review
- Gpr101 expression during early stages of murine development.Gene expression patterns : GEP · 2025Article
- A CRISPR mis-insertion in the Zic3 5'UTR inhibits in vivo translation and is predicted to result in formation of an mRNA stem-loop hairpin.Biology open · 2025Article
- Molecular mechanism, diagnosis, and treatment of VACTERL association.Frontiers in pediatrics · 2025Review
- Human-gained heart enhancers are associated with species-specific cardiac attributes.Nature cardiovascular research · 2022Article
- The genetic landscape of cardiovascular left-right patterning defects.Current opinion in genetics & development · 2022Review
- Left-handed cardiac looping by cell chirality is mediated by position-specific convergent extensions.Biophysical journal · 2021Article
- Loss of Zic3 impairs planar cell polarity leading to abnormal left-right signaling, heart defects and neural tube defects.Human molecular genetics · 2021Article
- Monoallelic Mutations inCirculation. Genomic and precision medicine · 2020Article
- Genetics of Congenital Heart Disease.Biomolecules · 2019Review
- Model organism data evolving in support of translational medicine.Lab animal · 2018Review
- A novel ZIC3 gene mutation identified in patients with heterotaxy and congenital heart disease.Scientific reports · 2018Article
- Evidence for the temporal regulation of insect segmentation by a conserved sequence of transcription factors.Development (Cambridge, England) · 2018Article
- ZIC3 in Heterotaxy.Advances in experimental medicine and biology · 2018Review
- Copy number variation as a genetic basis for heterotaxy and heterotaxy-spectrum congenital heart defects.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2016Article
- Changing Faces of Transcriptional Regulation Reflected by Zic3.Current genomics · 2015Article
- Article
- Genetic and functional analyses of ZIC3 variants in congenital heart disease.Human mutation · 2014Article
- MCTP2 is a dosage-sensitive gene required for cardiac outflow tract development.Human molecular genetics · 2013Article
- Heterotaxy-spectrum heart defects in Zic3 hypomorphic mice.Pediatric research · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Mutations in ZIC3 result in X-linked heterotaxy in humans, a syndrome consisting of left-right (L-R) patterning defects, midline abnormalities, and cardiac malformations. Similarly, loss of function of Zic3 in mouse results in abnormal L-R patterning and cardiac development. However, Zic3 null mice also exhibit defects in gastrulation, neural tube closure, and axial patterning, suggesting the hypothesis that Zic3 is necessary for proper convergent extension (C-E) morphogenesis. To further investigate the role of Zic3 in early embryonic development, we utilized two model systems, Xenopus laevis and zebrafish, and performed loss of function analysis using antisense morpholino-mediated gene knockdown. Both Xenopus and zebrafish demonstrated significant impairment of C-E in Zic3 morphants. L-R patterning was also disrupted, indicating that the role of Zic3 in L-R axis development is conserved across species. Correlation of L-R patterning and C-E defects in Xenopus suggests that early C-E defects may underlie L-R patterning defects at later stages, since Zic3 morphants with moderate to severe C-E defects exhibited an increase in laterality defects. Taken together, these results demonstrate a functional conservation of Zic3 in L-R patterning and uncover a previously unrecognized role for Zic3 in C-E morphogenesis during early vertebrate development.
Indexed as
Identifiers
What OpenQuestion holds
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.