ArticleThe Journal of biological chemistry2015
Zebrafish foxc1a plays a crucial role in early somitogenesis by restricting the expression of aldh1a2 directly.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 32 citations in OpenAlex.
- CRISPR-Cas9-mediated functional dissection of the foxc1 genomic region in zebrafish identifies critical conserved cis-regulatory elements.Human genomics · 2022Article
- Somite morphogenesis is required for axial blood vessel formation during zebrafish embryogenesis.eLife · 2022Article
- Mechanistic Insights into Axenfeld-Rieger Syndrome from ZebrafishInternational journal of molecular sciences · 2021Review
- Generation of a Triadin KnockOut Syndrome Zebrafish Model.International journal of molecular sciences · 2021Article
- Role of cell polarity dynamics and motility in pattern formation due to contact-dependent signalling.Journal of the Royal Society, Interface · 2021Article
- The Axenfeld-Rieger Syndrome GeneGenes · 2021Article
- Disruption of foxc1 genes in zebrafish results in dosage-dependent phenotypes overlapping Axenfeld-Rieger syndrome.Human molecular genetics · 2020Article
- MicroRNA-375 overexpression disrupts cardiac development of Zebrafish (Danio rerio) by targeting notch2.Protoplasma · 2020Article
- Axenfeld-Rieger syndrome-associated mutants of the transcription factor FOXC1 abnormally regulateThe Journal of biological chemistry · 2020Article
- Embryonic ethanol exposure alters expression of sox2 and other early transcripts in zebrafish, producing gastrulation defects.Scientific reports · 2020Article
- Plasma proteome profiling of freshwater and seawater life stages of rainbow trout (Oncorhynchus mykiss).PloS one · 2020Article
- LncRNA-SULT1C2A regulates Foxo4 in congenital scoliosis by targeting rno-miR-466c-5p through PI3K-ATK signalling.Journal of cellular and molecular medicine · 2019Article
- Elongation of Müllerian ducts and connection to urogenital sinus determine the borderline of uterine and vaginal development.Biochemistry and biophysics reports · 2019Article
- The transcription factor Foxc1a in zebrafish directly regulates expression ofThe Journal of biological chemistry · 2018Article
- A Conserved MicroRNA Regulatory Circuit Is Differentially Controlled during Limb/Appendage Regeneration.PloS one · 2016Article
- A new mib allele with a chromosomal deletion covering foxc1a exhibits anterior somite specification defect.Scientific reports · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Foxc1a is a member of the forkhead transcription factors. It plays an essential role in zebrafish somitogenesis. However, little is known about the molecular mechanisms underlying its controlling somitogenesis. To uncover how foxc1a regulates zebrafish somitogenesis, we generated foxc1a knock-out zebrafish using TALEN (transcription activator-like effector nuclease) technology. The foxc1a null embryos exhibited defective somites at early development. Analyses on the expressions of the key genes that control processes of somitogenesis revealed that foxc1a controlled early somitogenesis by regulating the expression of myod1. In the somites of foxc1a knock-out embryos, expressions of fgf8a and deltaC were abolished, whereas the expression of aldh1a2 (responsible for providing retinoic acid signaling) was significantly increased. Once the increased retinoic acid level in the foxc1a null embryos was reduced by knocking down aldh1a2, the reduced expression of myod1 was partially rescued by resuming expressions of fgf8a and deltaC in the somites of the mutant embryos. Moreover, a chromatin immunoprecipitation assay on zebrafish embryos revealed that Foxc1a bound aldh1a2 promoter directly. On the other hand, neither knocking down fgf8a nor inhibiting Notch signaling affected the expression of aldh1a2, although knocking down fgf8a reduced expression of deltaC in the somites of zebrafish embryos at early somitogenesis and vice versa. Taken together, our results demonstrate that foxc1a plays an essential role in early somitogenesis by controlling Fgf and Notch signaling through restricting the expression of aldh1a2 in paraxial mesoderm directly.
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.