scholarly journals Retinoic-acid signalling in node ectoderm and posterior neural plate directs left–right patterning of somitic mesoderm

2006 ◽  
Vol 8 (3) ◽  
pp. 271-277 ◽  
Author(s):  
Ioan Ovidiu Sirbu ◽  
Gregg Duester
Keyword(s):  
Retinoic Acid ◽  
Neural Plate ◽  
Retinoic Acid Signalling ◽  
Somitic Mesoderm

Distinct roles for Fgf, Wnt and retinoic acid in posteriorizing the neural ectoderm

Development ◽  
2002 ◽  
Vol 129 (18) ◽  
pp. 4335-4346 ◽  
Author(s):  
Tetsuhiro Kudoh ◽  
Stephen W. Wilson ◽  
Igor B. Dawid
Keyword(s):  
Retinoic Acid ◽  
Neural Plate ◽  
Neural Patterning ◽  
Knock Down ◽  
Complementary Pattern ◽  
Neural Ectoderm ◽  
Morpholino Oligonucleotides ◽  
And Function

Early neural patterning in vertebrates involves signals that inhibit anterior (A) and promote posterior (P) positional values within the nascent neural plate. In this study, we have investigated the contributions of, and interactions between, retinoic acid (RA), Fgf and Wnt signals in the promotion of posterior fates in the ectoderm. We analyze expression and function of cyp26/P450RAI, a gene that encodes retinoic acid 4-hydroxylase, as a tool for investigating these events. Cyp26 is first expressed in the presumptive anterior neural ectoderm and the blastoderm margin at the late blastula. When the posterior neural gene hoxb1b is expressed during gastrulation, it shows a strikingly complementary pattern to cyp26. Using these two genes, as well as otx2 and meis3 as anterior and posterior markers, we show that Fgf and Wnt signals suppress expression of anterior genes, including cyp26. Overexpression of cyp26 suppresses posterior genes, suggesting that the anterior expression of cyp26 is important for restricting the expression of posterior genes. Consistent with this, knock-down of cyp26 by morpholino oligonucleotides leads to the anterior expansion of posterior genes. We further show that Fgf- and Wnt-dependent activation of posterior genes is mediated by RA, whereas suppression of anterior genes does not depend on RA signaling. Fgf and Wnt signals suppress cyp26 expression, while Cyp26 suppresses the RA signal. Thus, cyp26 has an important role in linking the Fgf, Wnt and RA signals to regulate AP patterning of the neural ectoderm in the late blastula to gastrula embryo in zebrafish.

Genesis and prevention of spinal neural tube defects in the curly tail mutant mouse: involvement of retinoic acid and its nuclear receptors RAR-beta and RAR-gamma

Development ◽  
1995 ◽  
Vol 121 (3) ◽  
pp. 681-691
Author(s):  
W.H. Chen ◽  
G.M. Morriss-Kay ◽  
A.J. Copp
Keyword(s):  
Retinoic Acid ◽  
Neural Tube ◽  
Neural Tube Defects ◽  
In Situ Hybridisation ◽  
Tail Bud ◽  
Retinoic Acid Signalling ◽  
All Trans Retinoic Acid ◽  
Posterior Neuropore ◽  
Computerised Image Analysis ◽  
Curly Tail

A role for all-trans-retinoic acid in spinal neurulation is suggested by: (1) the reciprocal domains of expression of the retinoic acid receptors RAR-beta and RAR-gamma in the region of the closed neural tube and open posterior neuropore, respectively, and (2) the preventive effect of maternally administered retinoic acid (5 mg/kg) on spinal neural tube defects in curly tail (ct/ct) mice. Using in situ hybridisation and computerised image analysis we show here that in ct/ct embryos, RAR-beta transcripts are deficient in the hindgut endoderm, a tissue whose proliferation rate is abnormal in the ct mutant, and RAR-gamma transcripts are deficient in the tail bud and posterior neuropore region. The degree of deficiency of RAR-gamma transcripts is correlated with the severity of delay of posterior neuropore closure. As early as 2 hours following RA treatment at 10 days 8 hours post coitum, i.e. well before any morphogenetic effects are detectable, RAR-beta expression is specifically upregulated in the hindgut endoderm, and the abnormal expression pattern of RAR-gamma is also altered. These results suggest that the spinal neural tube defects which characterise the curly tail phenotype may be due to interaction between the ct gene product and one or more aspects of the retinoic acid signalling pathway.

scholarly journals Bmpr1bb is a novel gene involved in retinoic acid induced patterning of the zebrafish hindbrain

Eureka ◽  
2010 ◽  
Vol 1 (1) ◽  
pp. 11-19
Author(s):  
Braden Teitge
Keyword(s):  
Retinoic Acid ◽  
Bone Morphogenetic Proteins ◽  
Critical Role ◽  
Retinoic Acid Treatment ◽  
Teratogenic Effects ◽  
Downstream Target ◽  
Retinoic Acid Signalling ◽  
Uncharacterized Gene ◽  
Vitamin A Derivative

Retinoic acid signalling plays a critical role during zebrafish development.  The teratogenic effects of retinoic acid have been demonstrated by embryonic deformation resulting from insufficient or excessive levels of this vitamin A derivative.  During embryogenesis, bone morphogenetic proteins are closely linked to the physiological interpretation of RA gradients, particularly in the hindbrain.  We describe an uncharacterized gene, Bmpr1bb, as being significantly downregulated in response to retinoic acid treatment.  In situ expression demonstrates that Bmpr1bb is expressed ubiquitously at 10hpf, and is slowly downregulated until 48hpf where the expression is concentrated in the hindbrain.  We propose that Bmpr1bb is a downstream target of RA signalling, strongly downregulated during embryogenesis and specified to a specific region of the hindbrain.

scholarly journals Retinoic acid signalling during development

Development ◽  
2012 ◽  
Vol 139 (5) ◽  
pp. 843-858 ◽  
Author(s):  
M. Rhinn ◽  
P. Dolle
Keyword(s):  
Retinoic Acid ◽  
Retinoic Acid Signalling

scholarly journals Lens-regulated retinoic acid signalling controls expansion of the developing eye

Development ◽  
2018 ◽  
Vol 145 (19) ◽  
pp. dev167171 ◽  
Author(s):  
Jonathan N. Smith ◽  
Heather M. Walker ◽  
Hannah Thompson ◽  
J. Martin Collinson ◽  
Neil Vargesson ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Retinoic Acid Signalling

scholarly journals Liposomal delivery of hydrophobic RAMBAs provides good bioavailability and significant enhancement of retinoic acid signalling in neuroblastoma tumour cells

2020 ◽  
Vol 28 (6) ◽  
pp. 643-654 ◽  
Author(s):  
Maja Bilip ◽  
Shreya Shah ◽  
Mayuran Mathiyalakan ◽  
Aristides D. Tagalakis ◽  
Stephen L. Hart ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Tumour Cells ◽  
Significant Enhancement ◽  
Retinoic Acid Signalling ◽  
Liposomal Delivery

scholarly journals Acrylamide alters CREB and retinoic acid signalling pathways during differentiation of the human neuroblastoma SH-SY5Y cell line

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Kristina Attoff ◽  
Ylva Johansson ◽  
Andrea Cediel-Ulloa ◽  
Jessica Lundqvist ◽  
Rajinder Gupta ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Neuronal Differentiation ◽  
Cell Model ◽  
Camp Response Element Binding ◽  
Signalling Pathways ◽  
Human Neuroblastoma ◽  
Neuronal Markers ◽  
Retinoic Acid Signalling ◽  
Early Life Exposure ◽  
Element Binding Protein

Abstract Acrylamide (ACR) is a known neurotoxicant which crosses the blood–brain barrier, passes the placenta and has been detected in breast milk. Hence, early-life exposure to ACR could lead to developmental neurotoxicity. The aim of this study was to elucidate if non-cytotoxic concentrations of ACR alter neuronal differentiation by studying gene expression of markers significant for neurodevelopment in the human neuroblastoma SH-SY5Y cell model. Firstly, by using RNASeq we identified two relevant pathways that are activated during 9 days of retinoic acid (RA) induced differentiation i.e. RA receptor (RAR) activation and the cAMP response element-binding protein (CREB) signalling pathways. Next, by qPCR we showed that 1 and 70 µM ACR after 9 days exposure alter the expression of 13 out of 36 genes in the RAR activation pathway and 18 out of 47 in the CREB signalling pathway. Furthermore, the expression of established neuronal markers i.e. BDNF, STXBP2, STX3, TGFB1 and CHAT were down-regulated. Decreased protein expression of BDNF and altered ratio of phosphorylated CREB to total CREB were confirmed by western blot. Our results reveal that micromolar concentrations of ACR sustain proliferation, decrease neurite outgrowth and interfere with signalling pathways involved in neuronal differentiation in the SH-SY5Y cell model.

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