ArticleDevelopment (Cambridge, England)2005
Shifting boundaries of retinoic acid activity control hindbrain segmental gene expression.
Article in Development (Cambridge, England), 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 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
77 citing papers in PubMed, 182 citations in OpenAlex.
- Signaling mechanisms and dynamics governing the myocardial-epicardial fate switch during human cardiogenesis.Science advances · 2026Article
- The interplay between retinoic acid binding proteins and retinoic acid degrading enzymes in modulating retinoic acid concentrations.Current topics in developmental biology · 2025Review
- Early retinoic acid signaling organizes the body axis and defines domains for the forelimb and eye.Current topics in developmental biology · 2025Review
- Rewiring of the epigenome and chromatin architecture by exogenously induced retinoic acid signaling during zebrafish embryonic development.Nucleic acids research · 2024Article
- Sea lamprey enlightens the origin of the coupling of retinoic acid signaling to vertebrate hindbrain segmentation.Nature communications · 2024Article
- Zbtb16 mediates a switch between Fgf signalling regimes in the developing hindbrain.Development (Cambridge, England) · 2023Article
- Shared retinoic acid responsive enhancers coordinately regulate nascent transcription of Hoxb coding and non-coding RNAs in the developing mouse neural tube.Development (Cambridge, England) · 2023Article
- Retinoic acid, RARs and early development.Journal of molecular endocrinology · 2022Article
- Stepwise pluripotency transitions in mouse stem cells.EMBO reports · 2022Review
- Mechanisms of Feedback Regulation of Vitamin A Metabolism.Nutrients · 2022Review
- AOP Key Event Relationship report: Linking decreased retinoic acid levels with disrupted meiosis in developing oocytes.Current research in toxicology · 2022Article
- Segmentation and patterning of the vertebrate hindbrain.Development (Cambridge, England) · 2021Review
- Role of carotenoids and retinoids during heart development.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2020Review
- Retinoids and developmental neurotoxicity: Utilizing toxicogenomics to enhance adverse outcome pathways and testing strategies.Reproductive toxicology (Elmsford, N.Y.) · 2020Review
- Canonical Wnt/β-catenin activity and differential epigenetic marks direct sexually dimorphic regulation ofDevelopment (Cambridge, England) · 2020Article
- Regulating Retinoic Acid Availability during Development and Regeneration: The Role of the CYP26 Enzymes.Journal of developmental biology · 2020Review
- Article
- Retinoic acid signaling pathways.Development (Cambridge, England) · 2019Review
- RDH10 function is necessary for spontaneous fetal mouth movement that facilitates palate shelf elevation.Disease models & mechanisms · 2019Article
- An epiblast stem cell-derived multipotent progenitor population for axial extension.Development (Cambridge, England) · 2019Article
17 more citing papers are in PubMed but not listed here.
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 2 countries.
Funding
Abstract
Retinoic acid (RA) generated by Raldh2 in paraxial mesoderm is required for specification of the posterior hindbrain, including restriction of Hoxb1 expression to presumptive rhombomere 4 (r4). Hoxb1 expression requires 3' and 5' RA response elements for widespread induction up to r4 and for r3/r5 repression, but RA has previously been detected only from r5-r8, and vHnf1 is required for repression of Hoxb1 posterior to r4 in zebrafish. We demonstrate in mouse embryos that an RA signal initially travels from the paraxial mesoderm to r3, forming a boundary next to the r2 expression domain of Cyp26a1 (which encodes an RA-degrading enzyme). After Hoxb1 induction, the RA boundary quickly shifts to r4/r5, coincident with induction of Cyp26c1 in r4. A functional role for Cyp26c1 in RA degradation was established through examination of RA-treated embryos. Analysis of Raldh2-/- and vHnf1-/- embryos supports a direct role for RA in Hoxb1 induction up to r4 and repression in r3/r5, as well as an indirect role for RA in Hoxb1 repression posterior to r4 via RA induction of vHnf1 up to the r4/r5 boundary. Our findings suggest that Raldh2 and Cyp26 generate shifting boundaries of RA activity, such that r3-r4 receives a short pulse of RA and r5-r8 receives a long pulse of RA. These two pulses of RA activity function to establish expression of Hoxb1 and vHnf1 on opposite sides of the r4/r5 boundary.
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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.