Developmental Signals - Retinoic acid: Difference between revisions
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All-trans retinoic acid (atRA) is the transcriptionally active product of vitamin A and is known to play many roles in regulating embryo development. In the adult retinoid acid has additional signalling roles including [[Spermatozoa Development|spermatozoa maturation]]. | All-trans {{retinoic acid}} (atRA) is the transcriptionally active product of vitamin A and is known to play many roles in regulating embryo development. In the adult retinoid acid has additional signalling roles including [[Spermatozoa Development|spermatozoa maturation]]. | ||
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* '''Retinoic acid signaling and neuronal differentiation'''{{#pmid:25558812|PMID25558812}} "The identification of neurological symptoms caused by vitamin A deficiency pointed to a critical, early developmental role of vitamin A and its metabolite, retinoic acid (RA). The ability of RA to induce post-mitotic, neural phenotypes in various stem cells, in vitro, served as early evidence that RA is involved in the switch between proliferation and differentiation. In vivo studies have expanded this "opposing signal" model, and the number of primary neurons an embryo develops is now known to depend critically on the levels and spatial distribution of RA. The proneural and neurogenic transcription factors that control the exit of neural progenitors from the cell cycle and allow primary neurons to develop are partly elucidated, but the downstream effectors of RA receptor (RAR) signaling (many of which are putative cell cycle regulators) remain largely unidentified. The molecular mechanisms underlying RA-induced primary neurogenesis in anamniote embryos are starting to be revealed; however, these data have been not been extended to amniote embryos. There is growing evidence that bona fide RARs are found in some mollusks and other invertebrates, but little is known about their necessity or functions in neurogenesis. One normal function of RA is to regulate the cell cycle to halt proliferation, and loss of RA signaling is associated with dedifferentiation and the development of cancer. Identifying the genes and pathways that mediate cell cycle exit downstream of RA will be critical for our understanding of how to target tumor differentiation. Overall, elucidating the molecular details of RAR-regulated neurogenesis will be decisive for developing and understanding neural proliferation-differentiation switches throughout development." | * '''Retinoic acid signaling and neuronal differentiation'''{{#pmid:25558812|PMID25558812}} "The identification of neurological symptoms caused by vitamin A deficiency pointed to a critical, early developmental role of vitamin A and its metabolite, retinoic acid (RA). The ability of RA to induce post-mitotic, neural phenotypes in various stem cells, in vitro, served as early evidence that RA is involved in the switch between proliferation and differentiation. In vivo studies have expanded this "opposing signal" model, and the number of primary neurons an embryo develops is now known to depend critically on the levels and spatial distribution of RA. The proneural and neurogenic transcription factors that control the exit of neural progenitors from the cell cycle and allow primary neurons to develop are partly elucidated, but the downstream effectors of RA receptor (RAR) signaling (many of which are putative cell cycle regulators) remain largely unidentified. The molecular mechanisms underlying RA-induced primary neurogenesis in anamniote embryos are starting to be revealed; however, these data have been not been extended to amniote embryos. There is growing evidence that bona fide RARs are found in some mollusks and other invertebrates, but little is known about their necessity or functions in neurogenesis. One normal function of RA is to regulate the cell cycle to halt proliferation, and loss of RA signaling is associated with dedifferentiation and the development of cancer. Identifying the genes and pathways that mediate cell cycle exit downstream of RA will be critical for our understanding of how to target tumor differentiation. Overall, elucidating the molecular details of RAR-regulated neurogenesis will be decisive for developing and understanding neural proliferation-differentiation switches throughout development." | ||
* '''Visualization of an endogenous retinoic acid gradient across embryonic development'''{{#pmid:23563268|PMID23563268}} "In vertebrate development, the body plan is determined by primordial morphogen gradients that suffuse the embryo. Retinoic acid (RA) is an important morphogen involved in patterning the anterior-posterior axis of structures, including the hindbrain and paraxial mesoderm. RA diffuses over long distances, and its activity is spatially restricted by synthesizing and degrading enzymes. ...Live imaging of endogenous concentration gradients across embryonic development will allow the precise assignment of molecular mechanisms to developmental dynamics and will accelerate the application of approaches based on morphogen gradients to tissue engineering and regenerative medicine." | * '''Visualization of an endogenous retinoic acid gradient across embryonic development'''{{#pmid:23563268|PMID23563268}} "In vertebrate development, the body plan is determined by primordial morphogen gradients that suffuse the embryo. Retinoic acid (RA) is an important morphogen involved in patterning the anterior-posterior axis of structures, including the hindbrain and paraxial mesoderm. RA diffuses over long distances, and its activity is spatially restricted by synthesizing and degrading enzymes. ...Live imaging of endogenous concentration gradients across embryonic development will allow the precise assignment of molecular mechanisms to developmental dynamics and will accelerate the application of approaches based on morphogen gradients to tissue engineering and regenerative medicine." {{zebrafish}} | ||
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Revision as of 12:26, 19 April 2018
Embryology - 19 May 2024 Expand to Translate |
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Introduction
All-trans retinoic acid (atRA) is the transcriptionally active product of vitamin A and is known to play many roles in regulating embryo development. In the adult retinoid acid has additional signalling roles including spermatozoa maturation.
The compound has been used extensively postnatally in therapeutic treatments, for example in skin disease. As this compound also acts as a developmental signal, it has known teratogenic effects[2][3] following maternal to conceptus transfer.
Factor Links: AMH | hCG | BMP | sonic hedgehog | bHLH | HOX | FGF | FOX | Hippo | LIM | Nanog | NGF | Nodal | Notch | PAX | retinoic acid | SIX | Slit2/Robo1 | SOX | TBX | TGF-beta | VEGF | WNT | Category:Molecular |
| Category:Retinoic acid | Abnormal Development
Some Recent Findings
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More recent papers |
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This table allows an automated computer search of the external PubMed database using the listed "Search term" text link.
More? References | Discussion Page | Journal Searches | 2019 References | 2020 References Search term: Embryo Retinoic acid | Images <pubmed limit=5>Embryo Retinoic acid</pubmed> |
Organ Expression
Summary of Rar gene expression patterns in mouse developing organ systems.[8]
Endoderm
Chicken antero-posterior endoderm patterning[9]
- Links: Endoderm | Chicken Development
Fetal Gonad
Immunohistochemical localisation of retinoid receptor expression in the human fetal gonad[10]
Neural
Model retinoic acid extracellular signal-regulated kinase and Wnt pathway interactions[11]
RA Is Not Required for Radial Expansion of the Embryonic Cortex
References
- ↑ Paschaki M, Cammas L, Muta Y, Matsuoka Y, Mak SS, Rataj-Baniowska M, Fraulob V, Dollé P & Ladher RK. (2013). Retinoic acid regulates olfactory progenitor cell fate and differentiation. Neural Dev , 8, 13. PMID: 23829703 DOI.
- ↑ Collins MD & Mao GE. (1999). Teratology of retinoids. Annu. Rev. Pharmacol. Toxicol. , 39, 399-430. PMID: 10331090 DOI.
- ↑ Tzimas G & Nau H. (2001). The role of metabolism and toxicokinetics in retinoid teratogenesis. Curr. Pharm. Des. , 7, 803-31. PMID: 11375780
- ↑ Uribe RA, Hong SS & Bronner ME. (2018). Retinoic acid temporally orchestrates colonization of the gut by vagal neural crest cells. Dev. Biol. , 433, 17-32. PMID: 29108781 DOI.
- ↑ Rydeen AB & Waxman JS. (2016). Cyp26 Enzymes Facilitate Second Heart Field Progenitor Addition and Maintenance of Ventricular Integrity. PLoS Biol. , 14, e2000504. PMID: 27893754 DOI.
- ↑ Janesick A, Wu SC & Blumberg B. (2015). Retinoic acid signaling and neuronal differentiation. Cell. Mol. Life Sci. , 72, 1559-76. PMID: 25558812 DOI.
- ↑ Shimozono S, Iimura T, Kitaguchi T, Higashijima S & Miyawaki A. (2013). Visualization of an endogenous retinoic acid gradient across embryonic development. Nature , 496, 363-6. PMID: 23563268 DOI.
- ↑ Dollé P. (2009). Developmental expression of retinoic acid receptors (RARs). Nucl Recept Signal , 7, e006. PMID: 19471585 DOI.
- ↑ Bayha E, Jørgensen MC, Serup P & Grapin-Botton A. (2009). Retinoic acid signaling organizes endodermal organ specification along the entire antero-posterior axis. PLoS ONE , 4, e5845. PMID: 19516907 DOI.
- ↑ Childs AJ, Cowan G, Kinnell HL, Anderson RA & Saunders PT. (2011). Retinoic Acid signalling and the control of meiotic entry in the human fetal gonad. PLoS ONE , 6, e20249. PMID: 21674038 DOI.
- ↑ Lu J, Tan L, Li P, Gao H, Fang B, Ye S, Geng Z, Zheng P & Song H. (2009). All-trans retinoic acid promotes neural lineage entry by pluripotent embryonic stem cells via multiple pathways. BMC Cell Biol. , 10, 57. PMID: 19642999 DOI.
Reviews
Dubey A, Rose RE, Jones DR & Saint-Jeannet JP. (2018). Generating retinoic acid gradients by local degradation during craniofacial development: One cell's cue is another cell's poison. Genesis , 56, . PMID: 29330906 DOI.
Articles
Bozzo P, Chua-Gocheco A & Einarson A. (2011). Safety of skin care products during pregnancy. Can Fam Physician , 57, 665-7. PMID: 21673209
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Cite this page: Hill, M.A. (2024, May 19) Embryology Developmental Signals - Retinoic acid. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Developmental_Signals_-_Retinoic_acid
- © Dr Mark Hill 2024, UNSW Embryology ISBN: 978 0 7334 2609 4 - UNSW CRICOS Provider Code No. 00098G