Early morphological abnormalities in splotch mouse embryos and predisposition to gene- and retinoic acid-induced neural tube defects

Teratology ◽  
1983 ◽  
Vol 28 (3) ◽  
pp. 461-472 ◽  
Author(s):  
Ellen E. Dempsey ◽  
Daphne G. Trasler
Keyword(s):  
Retinoic Acid ◽  
Neural Tube ◽  
Neural Tube Defects ◽  
Mouse Embryos ◽  
Morphological Abnormalities

Perturbations in choline metabolism cause neural tube defects in mouse embryos in vitro

2002 ◽  
Vol 16 (6) ◽  
pp. 619-621 ◽  
Author(s):  
Melanie C. Fisher ◽  
Steven H. Zeisel ◽  
Mei-Heng Mar ◽  
Thomas W. Sadler
Keyword(s):  
Neural Tube ◽  
Neural Tube Defects ◽  
Mouse Embryos ◽  
Choline Metabolism

RNA-Seq analysis reveals candidate genes that may explain neural tube defects in mouse embryos lacking SR-BI

Placenta ◽  
2017 ◽  
Vol 51 ◽  
pp. 118-119
Author(s):  
N. Santander ◽  
C. Lizama ◽  
A. Quiroz ◽  
A. Rigotti ◽  
D. Busso
Keyword(s):  
Candidate Genes ◽  
Neural Tube ◽  
Neural Tube Defects ◽  
Mouse Embryos ◽  
Rna Seq

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.

Neural tube development in mutant (curly tail) and normal mouse embryos: the timing of posterior neuropore closure in vivo and in vitro

Development ◽  
1982 ◽  
Vol 69 (1) ◽  
pp. 151-167
Author(s):  
A. J. Copp ◽  
M. J. Seller ◽  
P. E. Polani
Keyword(s):  
Neural Tube ◽  
Neural Tube Defects ◽  
Mouse Embryos ◽  
Injection Technique ◽  
Posterior Neuropore ◽  
Curly Tail ◽  
Mechanisms Of Development ◽  
Delayed Closure

A dye-injection technique has been used to determine the developmental stage at which posterior neuropore (PNP) closure occurs in normal and mutant curly tail mouse embryos. In vivo, the majority of non-mutant embryos undergo PNP closure between 30 and 34 somites whereas approximately 50% of all mutant embryos show delayed closure, and around 20% maintain an open PNP even at advanced stages of development. A similar result has been found for embryos developing in vitro from the headfold stage. Later in development, 50–60% of mutant embryos in vivo develop tail flexion defects, and 15–20% lumbosacral myeloschisis. This supports the view that delayed PNP closure is the main developmental lesion leading to the appearance of caudal neural tube defects in curly tail mice. The neural tube is closed in the region of tail flexion defects, but it is locally overexpanded and abnormal in position. The significance of these observations is discussed in relation to possible mechanisms of development of lumbosacral and caudal neural tube defects. This paper constitutes the first demonstration of the development of a genetically induced malformation in vitro.

Common hierarchies of susceptibility to the induction of neural tube defects in mouse embryos by valproic acid and its 4-propyl-4-pentenoic acid metabolite

Teratology ◽  
1988 ◽  
Vol 38 (4) ◽  
pp. 313-320 ◽  
Author(s):  
Richard H. Finnell ◽  
Gregory D. Bennett ◽  
Steven B. Karras ◽  
Virginia K. Mohl
Keyword(s):  
Valproic Acid ◽  
Neural Tube ◽  
Neural Tube Defects ◽  
Mouse Embryos ◽  
Acid Metabolite
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