|
|
|
|
|
|
|
||||
| Home Help Feedback Subscriptions Archive Search Table of Contents | ||||
Development, Vol 108, Issue 1 73-81, Copyright © 1990 by Company of Biologists
JOURNAL ARTICLES |
AJ Alles and KK Sulik
Department of Cell Biology and Anatomy, University of North Carolina Chapel Hill 27599.
Treatment of C57Bl/6J mice with three successive doses of all-trans retinoic acid (28 mg kg-1 body weight) on 8 day, 6 h (8d,6h), 8d,12h, and 8d,18h of gestation resulted in a high incidence (79%, 31/39 fetuses) of spina bifida with myeloschisis (spina bifida aperta) in near term fetuses. Twelve hours following the last maternal dose (9d,6h), the caudal aspects of treated embryos, were abnormal, with eversion of the neural plate at the posterior neuropore, as compared to its normal concavity in comparably staged control specimens. This eversion persisted in affected embryos through the time that the posterior neuropore should normally close. The distribution of cell death in control and experimental embryos was determined using vital staining with Nile blue sulphate and with routine histological techniques. Twelve hours following the maternal dosing regimen, experimental embryos showed evidence of excessive cell death, predominantly in the mesenchyme associated with the primitive streak and in the endoderm of the tail gut, both of which are readily identifiable sites of physiological cell death at this stage of development. In addition, the presumptive trunk neural crest cells located in the dorsal midline, cranial to the posterior neuropore, exhibited a marked amount of cell death in the experimental embryos. We propose that the major factor in the generation of spina bifida in this model is excessive cell death in the tail gut and mesenchyme ventral to the neuroepithelium of the posterior neuropore.(ABSTRACT TRUNCATED AT 250 WORDS)
This article has been cited by other articles:
|
|
 |
|
  R. L. Y. Wong, B. J. Wlodarczyk, K. S. Min, M. L. Scott, S. Kartiko, W. Yu, M. Y. Merriweather, P. Vogel, B. P. Zambrowicz, and R. H. Finnell Mouse Fkbp8 activity is required to inhibit cell death and establish dorso-ventral patterning in the posterior neural tube Hum. Mol. Genet., February 14, 2008; 17(4): 587 - 601. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J.-P. Chambon, A. Nakayama, K. Takamura, A. McDougall, and N. Satoh ERK- and JNK-signalling regulate gene networks that stimulate metamorphosis and apoptosis in tail tissues of ascidian tadpoles Development, March 15, 2007; 134(6): 1203 - 1219. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Abu-Abed, P. Dolle, D. Metzger, C. Wood, G. MacLean, P. Chambon, and M. Petkovich Developing with lethal RA levels: genetic ablation of Rarg can restore the viability of mice lacking Cyp26a1 Development, April 1, 2003; 130(7): 1449 - 1459. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G Deutsch, J Jung, M Zheng, J Lora, and K. Zaret A bipotential precursor population for pancreas and liver within the embryonic endoderm Development, January 3, 2001; 128(6): 871 - 881. [Abstract] [PDF]
|
|
|
|
 |
|
 H. B. Samat and J. H. Menkes How to Construct a Neural Tube J Child Neurol, February 1, 2000; 15(2): 110 - 124. [PDF]
|
|
|
|
 |
|
 J. X. Kang, J. Bell, R. L. Beard, and R. A. S. Chandraratna Mannose 6-Phosphate/Insulin-like Growth Factor II Receptor Mediates the Growth-Inhibitory Effects of Retinoids Cell Growth Differ., August 1, 1999; 10(8): 591 - 600. [Abstract] [Full Text]
|
|
|
|
 |
|
 N. Ferrari, M. Pfahl, and G. Levi Retinoic Acid Receptor gamma 1 (RARgamma 1) Levels Control RARbeta 2 Expression in SK-N-BE2(c) Neuroblastoma Cells and Regulate a Differentiation-Apoptosis Switch Mol. Cell. Biol., November 1, 1998; 18(11): 6482 - 6492. [Abstract] [Full Text]
|
|
|
|
|
|
E Ruberte, V Friederich, P Chambon, and G Morriss-Kay Retinoic acid receptors and cellular retinoid binding proteins. III. Their differential transcript distribution during mouse nervous system development Development, January 5, 1993; 118(1): 267 - 282. [Abstract] [PDF]
|
|
|
|
 |
|
 H L Sive, B W Draper, R M Harland, and H Weintraub Identification of a retinoic acid-sensitive period during primary axis formation in Xenopus laevis. Genes & Dev., June 1, 1990; 4(6): 932 - 942. [Abstract] [PDF]
|
|
