scholarly journals What's retinoic acid got to do with it? Retinoic acid regulation of the neural crest in craniofacial and ocular development

genesis ◽  
2019 ◽  
pp. e23308 ◽  
Author(s):  
Antionette L. Williams ◽  
Brenda L. Bohnsack
Keyword(s):  
Retinoic Acid ◽  
Neural Crest ◽  
Ocular Development

scholarly journals Retinoic Acid Accelerates the Specification of Enteric Neural Progenitors from In-Vitro-Derived Neural Crest

2020 ◽  
Vol 15 (3) ◽  
pp. 557-565
Author(s):  
Thomas J.R. Frith ◽  
Antigoni Gogolou ◽  
James O.S. Hackland ◽  
Zoe A. Hewitt ◽  
Harry D. Moore ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Neural Crest ◽  
Neural Progenitors

Temporally-regulated retinoic acid depletion produces specific neural crest, ocular and nervous system defects

Development ◽  
1997 ◽  
Vol 124 (16) ◽  
pp. 3111-3121 ◽  
Author(s):  
E.D. Dickman ◽  
C. Thaller ◽  
S.M. Smith
Keyword(s):  
Nervous System ◽  
Retinoic Acid ◽  
Neural Crest ◽  
Female Rats ◽  
Retinoid Receptor ◽  
Knock Out ◽  
The Face ◽  
Normal Males ◽  
Temporal Events ◽  
Null Mutant Mice

Both retinoid receptor null mutants and classic nutritional deficiency studies have demonstrated that retinoids are essential for the normal development of diverse embryonic structures (e.g. eye, heart, nervous system, urogenital tract). Detailed analysis of retinoid-modulated events is hampered by several limitations of these models, including that deficiency or null mutation is present throughout gestation, making it difficult to isolate primary effects, and preventing analysis beyond embryolethality. We developed a mammalian model in which retinoid-dependent events are documented during distinct targeted windows of embryogenesis. This was accomplished through the production of vitamin A-depleted (VAD) female rats maintained on sufficient oral retinoic acid (RA) for growth and fertility. After mating to normal males, these RA-sufficient/VAD females were given oral RA doses which allowed for gestation in an RA-sufficient state; embryogenesis proceeded normally until retinoids were withdrawn dietarily to produce a sudden, acute retinoid deficiency during a selected gestational window. In this trial, final RA doses were administered on E11.5, vehicle at E12.5, and embryos analyzed on E13.5; during this 48 hour window, the last RA dose was metabolized and embryos progressed in a retinoid-deficient state. RA-sufficient embryos were normal. Retinoid-depleted embryos exhibited specific malformations of the face, neural crest, eyes, heart, and nervous system. Some defects were phenocopies of those seen in null mutant mice for RXR alpha(−/−), RXR alpha(−/−)/RAR alpha(−/−), and RAR alpha(−/−)/RAR gamma(−/−), confirming that RA transactivation of its nuclear receptors is essential for normal embryogenesis. Other defects were unique to this deficiency model, showing that complete ligand ‘knock-out’ is required to see those retinoid-dependent events previously concealed by receptor functional redundancy, and reinforcing that retinoid receptors have separate yet overlapping contributions in the embryo. This model allows for precise targeting of retinoid form and deficiency to specific developmental windows, and will facilitate studies of distinct temporal events.

Retinoid-binding protein distribution in the developing mammalian nervous system

Development ◽  
1990 ◽  
Vol 109 (1) ◽  
pp. 75-80 ◽  
Author(s):  
M. Maden ◽  
D.E. Ong ◽  
F. Chytil
Keyword(s):  
Nervous System ◽  
Retinoic Acid ◽  
Neural Crest ◽  
Motor Neurons ◽  
Neural Tube ◽  
Binding Protein ◽  
Sympathetic Ganglia ◽  
Retinol Binding Protein ◽  
Otic Vesicle ◽  
Protein Distribution

We have analysed the distribution of cellular retinol-binding protein (CRBP) and cellular retinoic acid-binding protein (CRABP) in the day 8.5-day 12 mouse and rat embryo. CRBP is localised in the heart, gut epithelium, notochord, otic vesicle, sympathetic ganglia, lamina terminalis of the brain, and, most strikingly, in a ventral stripe across the developing neural tube in the future motor neuron region. This immunoreactivity remains in motor neurons and, at later stages, motor axons are labelled in contrast to unlabelled sensory axons. CRABP is localised to the neural crest cells, which are particularly noticeable streaming into the branchial arches. At later stages, neural crest derivatives such as Schwann cells, cells in the gut wall and sympathetic ganglia are immunoreactive. An additional area of CRABP-positive cells are neuroblasts in the mantle layer of the neural tube, which subsequently appear to be the axons and cell bodies of the commissural system. Since retinol and retinoic acid are the endogenous ligands for these binding proteins, we propose that retinoids may play a role in the development and differentiation of the mammalian nervous system and may interact with certain homoeobox genes whose transcripts have also been localised within the nervous system.

Development of the spatial pattern of retinoic acid receptor-beta transcripts in embryonic chick facial primordia

Development ◽  
1992 ◽  
Vol 114 (3) ◽  
pp. 805-813
Author(s):  
A. Rowe ◽  
J.M. Richman ◽  
P.M. Brickell
Keyword(s):  
Retinoic Acid ◽  
Neural Crest ◽  
Retinoic Acid Receptor ◽  
In Situ Hybridisation ◽  
Acid Receptor ◽  
Retinoic Acid Receptor Beta ◽  
Low Levels ◽  
Cranial Neural Crest Cells ◽  
Receptor Beta

Retinoic acid causes a range of embryonic defects, including craniofacial abnormalities, in both birds and mammals and is believed to have a number of roles in normal development. We have previously shown that the distribution of retinoic acid receptor-beta (RAR-beta) transcripts is spatially restricted within the neural-crest-derived upper beak primordia of the chick embryo. We have now used in situ hybridisation to trace the distribution of RAR-beta transcripts during the migration of cranial neural crest cells and during formation of these primordia. RAR-beta transcripts were present in a subset of migrating neural-crest-derived cells in the head of the stage 10 embryo. These cells were situated in pathways followed by cells that migrate from the neural crest overlying the posterior prosencephalic/anterior mesencephalic region of the developing brain. Cells containing RAR-beta transcripts accumulated around the developing eyes and in the regions of the ventral head from which the upper beak primordia later develop. We mapped the distribution of RAR-beta transcripts as the facial primordia were forming, with particular reference to the development of the maxillary primordia. We found that these form in a region of the ventral head that includes the boundary between regions of high and low levels of RAR-beta transcripts. The boundary between these two groups of cells persisted as the maxillary primordia developed.(ABSTRACT TRUNCATED AT 250 WORDS)

Retinoic acid synthesis and hindbrain patterning in the mouse embryo

Development ◽  
2000 ◽  
Vol 127 (1) ◽  
pp. 75-85 ◽  
Author(s):  
K. Niederreither ◽  
J. Vermot ◽  
B. Schuhbaur ◽  
P. Chambon ◽  
P. Dolle
Keyword(s):  
Retinoic Acid ◽  
Neural Crest ◽  
Hox Genes ◽  
Receptor Gene ◽  
Acid Synthesis ◽  
Branchial Arch ◽  
Eph Receptor ◽  
Caudal Portion ◽  
Midbrain Region ◽  
Broad Domain

Targeted disruption of the murine retinaldehyde dehydrogenase 2 (Raldh2) gene precludes embryonic retinoic acid (RA) synthesis, leading to midgestational lethality (Niederreither, K., Subbarayan, V., Dolle, P. and Chambon, P. (1999). Nature Genet. 21, 444–448). We describe here the effects of this RA deficiency on the development of the hindbrain and associated neural crest. Morphological segmentation is impaired throughout the hindbrain of Raldh2−/− embryos, but its caudal portion becomes preferentially reduced in size during development. Specification of the midbrain region and of the rostralmost rhombomeres is apparently normal in the absence of RA synthesis. In contrast, marked alterations are seen throughout the caudal hindbrain of mutant embryos. Instead of being expressed in two alternate rhombomeres (r3 and r5), Krox20 is expressed in a single broad domain, correlating with an abnormal expansion of the r2-r3 marker Meis2. Instead of forming a defined r4, Hoxb1- and Wnt8A-expressing cells are scattered throughout the caudal hindbrain, whereas r5/r8 markers such as kreisler or group 3/4 Hox genes are undetectable or markedly downregulated. Lack of alternate Eph receptor gene expression could explain the failure to establish rhombomere boundaries. Increased apoptosis and altered migratory pathways of the posterior rhombencephalic neural crest cells are associated with impaired branchial arch morphogenesis in mutant embryos. We conclude that RA produced by the embryo is required to generate posterior cell fates in the developing mouse hindbrain, its absence leading to an abnormal r3 (and, to a lesser extent, r4) identity of the caudal hindbrain cells.

scholarly journals Semaphorin3A regulates neural crest migration during ocular development

2008 ◽  
Vol 319 (2) ◽  
pp. 541-542
Author(s):  
Peter Y. Lwigale ◽  
Marianne Bronner-Fraser
Keyword(s):  
Neural Crest ◽  
Ocular Development ◽  
Neural Crest Migration

Saturable Accumulation of Retinoic Acid in Neural and Neural Crest Derived Cells in Early Embryonic Development

1987 ◽  
Vol 10 (3) ◽  
pp. 212-223 ◽  
Author(s):  
L. Dencker ◽  
R. d’Argy ◽  
B.R.G. Danielsson ◽  
H. Ghantous ◽  
G.O. Sperber
Keyword(s):  
Retinoic Acid ◽  
Embryonic Development ◽  
Neural Crest ◽  
Early Embryonic Development
Sign in / Sign up

Export Citation Format

Share Document