ArticleDevelopmental biology2015
Excessive feedback of Cyp26a1 promotes cell non-autonomous loss of retinoic acid signaling.
Article in Developmental biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
31 citing papers in PubMed, 42 citations in OpenAlex.
- Tbx1-dependent and independent pathways promote six gene expression downstream of retinoic acid signaling to determine cardiomyocyte number in zebrafish.Developmental biology · 2025Article
- Migration of Kupffer's vesicle-derived cells is essential for tail morphogenesis in zebrafish embryos.Development (Cambridge, England) · 2025Article
- Zebrafish as a Versatile Model for Cardiovascular Research: Peering into the Heart of the Matter.Cells · 2025Review
- Vitamin A deficiency and male-specific effects on heart function in mice.Biochemical and biophysical research communications · 2025Article
- Feedback regulation of retinaldehyde reductase DHRS3, a critical determinant of retinoic acid homeostasis.FEBS letters · 2025Article
- Zebrafish as a Model to Study Retinoic Acid Signaling in Development and Disease.Biomedicines · 2023Review
- Effects of all-trans and 9-cis retinoic acid on differentiating human neural stem cells in vitro.Toxicology · 2023Article
- Symptomatic and asymptomatic domoic acid exposure in zebrafish (Danio rerio) revealed distinct non-overlapping gene expression patterns in the brain.Aquatic toxicology (Amsterdam, Netherlands) · 2022Article
- Mesoderm induction and patterning: Insights from neuromesodermal progenitors.Seminars in cell & developmental biology · 2022Review
- Mechanisms of Feedback Regulation of Vitamin A Metabolism.Nutrients · 2022Review
- Patterning of vertebrate cardiac progenitor fields by retinoic acid signaling.Genesis (New York, N.Y. : 2000) · 2021Review
- Segmentation and patterning of the vertebrate hindbrain.Development (Cambridge, England) · 2021Review
- Retinoic Acid Fluctuation Activates an Uneven, Direction-Dependent Network-Wide Robustness Response in Early Embryogenesis.Frontiers in cell and developmental biology · 2021Article
- Role of carotenoids and retinoids during heart development.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2020Review
- Mesoderm patterning by a dynamic gradient of retinoic acid signalling.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2020Review
- Regulating Retinoic Acid Availability during Development and Regeneration: The Role of the CYP26 Enzymes.Journal of developmental biology · 2020Review
- Modulation of retinoid signaling: therapeutic opportunities in organ fibrosis and repair.Pharmacology & therapeutics · 2020Review
- New Insights into the Control of Cell Fate Choices and Differentiation by Retinoic Acid in Cranial, Axial and Caudal Structures.Biomolecules · 2019Review
- Undifferentiated spermatogonia regulateFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Recent insights on the role and regulation of retinoic acid signaling during epicardial development.Genesis (New York, N.Y. : 2000) · 2019Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 3 countries.
Funding
Abstract
Teratogenic levels of retinoic acid (RA) signaling can cause seemingly contradictory phenotypes indicative of both increases and decreases of RA signaling. However, the mechanisms underlying these contradictory phenotypes are not completely understood. Here, we report that using a hyperactive RA receptor to enhance RA signaling in zebrafish embryos leads to defects associated with gain and loss of RA signaling. While the gain-of-function phenotypes arise from an initial increase in RA signaling, using genetic epistasis analysis we found that the loss-of-function phenotypes result from a clearing of embryonic RA that requires a rapid and dramatic increase in cyp26a1 expression. Thus, the sensitivity of cyp26a1 expression to increased RA signaling causes an overcompensation of negative feedback and loss of embryonic RA signaling. Additionally, we used blastula transplantation experiments to test if Cyp26a1, despite its cellular localization, can limit RA exposure to neighboring cells. We find that enhanced Cyp26a1 expression limits RA signaling in the local environment, thus providing the first direct evidence that Cyp26 enzymes can have cell non-autonomous consequences on RA levels within tissues. Therefore, our results provide novel insights into the teratogenic mechanisms of RA signaling and the cellular mechanisms by which Cyp26a1 expression can shape a RA gradient.
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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.