scholarly journals Retinoic acid is required for specification of the ventral eye field and for Rathke's pouch in the avian embryo

2007 ◽  
Vol 51 (3) ◽  
pp. 191-200 ◽  
Author(s):  
Malcolm Maden ◽  
Aida Blentic ◽  
Susan Reijntjes ◽  
Sophie Seguin ◽  
Emily Gale ◽  
...  
2010 ◽  
pp. OR38-3-OR38-3
Author(s):  
Carles Gaston-Massuet ◽  
Cynthia L Andoniadou ◽  
Massimo Signore ◽  
Sajutha Jayakody ◽  
Nicoletta Charolidi ◽  
...  

Development ◽  
2002 ◽  
Vol 129 (9) ◽  
pp. 2271-2282 ◽  
Author(s):  
Felix A. Mic ◽  
Robert J. Haselbeck ◽  
Arnold E. Cuenca ◽  
Gregg Duester

Retinoid control of vertebrate development depends upon tissue-specific metabolism of retinol to retinoic acid (RA). The RA biosynthetic enzyme RALDH2 catalyzes much, but not all, RA production in mouse embryos, as revealed here with Raldh2 null mutants carrying an RA-responsive transgene. Targeted disruption of Raldh2 arrests development at midgestation and eliminates all RA synthesis except that associated with Raldh3 expression in the surface ectoderm of the eye field. Conditional rescue of Raldh2–/– embryos by limited maternal RA administration allows development to proceed and results in the establishment of additional sites of RA synthesis linked to Raldh1 expression in the dorsal retina and to Raldh3 expression in the ventral retina, olfactory pit and urinary tract. Unexpectedly, conditionally rescued Raldh2–/– embryos also possess novel sites of RA synthesis in the neural tube and heart that do not correspond to expression of Raldh1-3. RA synthesis in the mutant neural tube was localized in the spinal cord, posterior hindbrain and portions of the midbrain and forebrain, whereas activity in the mutant heart was localized in the conotruncus and sinus venosa. In the posterior hindbrain, this novel RA-generating activity was expressed during establishment of rhombomeric boundaries. In the spinal cord, the novel activity was localized in the floorplate plus in the intermediate region where retinoid-dependent interneurons develop. These novel RA-generating activities in the neural tube and heart fill gaps in our knowledge of how RA is generated spatiotemporally and may, along with Raldh1 and Raldh3, contribute to rescue of Raldh2–/– embryos by producing RA locally.


Development ◽  
1996 ◽  
Vol 122 (1) ◽  
pp. 195-204 ◽  
Author(s):  
G.A. Hyatt ◽  
E.A. Schmitt ◽  
N. Marsh-Armstrong ◽  
P. McCaffery ◽  
U.C. Drager ◽  
...  

The developing eye is known to be rich in retinoic acid (RA), and perturbations in RA levels during formation of the optic primordia, as well as RA receptor mutations, cause retinal malformations, especially in ventral eye regions. To test the hypothesis that RA plays a role in the establishment of ventral retinal characteristics, we examined several dorsal and ventral ocular markers in RA-treated zebrafish. The optic stalk represents the ventral-most region of the early eye field. During normal development, the optic stalks constrict, decreasing in width and are gradually replaced by the optic nerve. Systemic high RA levels cause an expansion in the optic stalk with an increased cell content and a patent lumen. In addition, the stalks do not constrict and persist into later stages of development indicating an enhancement of early ventral eye characteristics. Expression of the transcription factor pax[b], normally confined to the ventral retina, expands into the dorsal retina following RA treatment, whereas msh[c], normally expressed in the dorsal retinal pole, disappears. Activity of an aldehyde dehydrogenase that normally occupies the dorsal third of the retina is reduced or abolished following high systemic RA. When a localized RA source, an RA-soaked bead, is placed next to the developing eye, a fissure resembling the choroid fissure appears in the eye facing the bead. Taken together, these observations suggest that RA is involved in the determination of the ventral retina.


1979 ◽  
Vol 207 (3) ◽  
pp. 351-366 ◽  
Author(s):  
Antone G. Jacobson ◽  
David M. Miyamoto ◽  
S.-H. Mai

JAMA ◽  
1978 ◽  
Vol 240 (5) ◽  
pp. 471-473 ◽  
Author(s):  
K. M. Trokoudes

1980 ◽  
Vol 17 (4) ◽  
pp. 406-421 ◽  
Author(s):  
R. Müller-Peddinghaus ◽  
M. F. El Etreby ◽  
J. Siefert ◽  
M. Ranke

Pituitary Dwarfism in a German Shepherd Dog Pituitary dwarfism has been described in more than 20 German shepherd dogs. Some cases probably were caused by persistent cysts of Rathke's pouch. This is the first histopathological, immunohistochemical and endocrinological study. A 13-month-old, 7-kg, dwarf purebred German shepherd bitch with alopecia and hyper pigmentation was admitted to the clinic for euthanasia. Retardation of growth was noticed when the dog was about two months old. No littermates had this condition. Two subsequent breedings from the same parents produced normal offspring. The clinical parameters in our dog (hematology, function of liver and kidney) were normal. Grossly, the pituitary gland had small and large multiple cysts, which light microscopy showed to be exclusively within the adenohypophysis. The latter had pressure atrophy, and immunohistochemically showed only remnants of the hormone-producing cells (growth hormone—GH; prolactin—PRL; thyrotropin—TSH; luteinizing hormone—LH; adrenocorticotrophin—ACTH/MSH). The thyroid was relatively small, and histologically showed focally resting follicles without lumen. Endocrinological studies showed a surprisingly high value for serum growth hormone (cGH 4.1 ng/ml; normal range 1.8–3.8 ng/ml as determined by a specific homologous radioimmunoassay) and a pathologically low serum somatomedin (SM 0.132; normal value more than 0.50 unit/ml, determined by 35S incorporation in piglet rib cartilage). Hypothyroidism was verified by a low T4 binding value (T4 0.9 μg/100 ml; normal 4.1 ± 0.9 μg/100 ml) and a low thyroid binding index (TBI 0.54; normal 0.61 ± 0.05). While ACTH was lowered (ACTH <10 pg/ml; normal 74–210 pg/ml), cortisol was normal (0.81 μg/100 ml; normal 0.5–2.5 μg/100 ml). Pituitary dwarfism in the 13-month-old bitch can be ascribed to the persistence of one end of the ductus craniopharyngeus. Rathke's pouch. Pressure atrophy of the adenohypophysis led to the loss of most of the hormone-producing tissue. An increase in growth hormone with lowered somatomedin raises questions. We have no conclusive explanation for this, due to the present lack of knowledge of how growth is regulated. High growth hormone and low somatomedin values are found in Laron's syndrome in infants. The literature indicates that pituitary dwarfism in German shepherd dogs may be a hereditary autosomal recessive trait.


2011 ◽  
Vol 346 (3) ◽  
pp. 339-346 ◽  
Author(s):  
Hideji Yako ◽  
Takako Kato ◽  
Saishu Yoshida ◽  
Kinji Inoue ◽  
Yukio Kato

1983 ◽  
Vol 97 (1) ◽  
pp. 81-88 ◽  
Author(s):  
Shigeo Daikoku ◽  
Mika Chikamori ◽  
Tohru Adachi ◽  
Yoshihito Okamura ◽  
Tohru Nishiyama ◽  
...  

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