scholarly journals Early Stages of Notochord and Floor Plate Development in the Chick Embryo Defined by Normal and Induced Expression of HNF-3β

1995 ◽  
Vol 170 (2) ◽  
pp. 299-313 ◽  
Author(s):  
A.Ruiz i Altaba ◽  
M. Placzek ◽  
M. Baldassare ◽  
J. Dodd ◽  
T.M. Jessell
Keyword(s):  
Chick Embryo ◽  
Floor Plate ◽  
Induced Expression ◽  
Early Stages

Stereological study on the mode of optic cup expansion and the accumulation of mitoses in the early stages of chick embryo development

1988 ◽  
Vol 222 (4) ◽  
pp. 401-407 ◽  
Author(s):  
Ruth Calvente ◽  
Ramón Carmona ◽  
Francisco Abadí-Molina ◽  
Francisco Abadía-Fenoll
Keyword(s):  
Chick Embryo ◽  
Embryo Development ◽  
Early Stages ◽  
Optic Cup

Special Problems of Experimenting in ovo on the Early Chick Embryo, and a Solution

Development ◽  
1960 ◽  
Vol 8 (4) ◽  
pp. 369-375
Author(s):  
P. H. S. Silver
Keyword(s):  
Chick Embryo ◽  
Short Term ◽  
Stages Of Development ◽  
In Ovo ◽  
Technical Problems ◽  
Early Chick Embryo ◽  
In Vitro Methods ◽  
Early Stages

It seems to be generally accepted that experimenting in ovo on the chick during the early stages of development (up to about 48 hours) is fraught with the greatest difficulty. After about this time no serious technical problems arise and a high proportion of successful results can be expected. It is natural to ask why there should be this change-over from extreme difficulty to reasonable simplicity. New (1955) attributed to this ‘inaccessibility of the chick embryo in the egg’ the invention of his own and many other in vitro methods during the last 30 years. There is no doubt that, when short-term experiments only are required, in vitro methods will probably always be preferred. But all in vitro methods suffer from the disadvantage that the embryo cannot be expected to survive for more than 48 hours or so after explantation.

Ectodermal patterning in the avian embryo: epidermis versus neural plate

Development ◽  
1999 ◽  
Vol 126 (1) ◽  
pp. 63-73 ◽  
Author(s):  
E. Pera ◽  
S. Stein ◽  
M. Kessel
Keyword(s):  
Chick Embryo ◽  
Neural Crest ◽  
Plate Boundary ◽  
Homeobox Gene ◽  
Primitive Streak ◽  
Neural Plate ◽  
Avian Embryo ◽  
Neural Fate ◽  
Early Stages ◽  
Two Factors

Ectodermal patterning of the chick embryo begins in the uterus and continues during gastrulation, when cells with a neural fate become restricted to the neural plate around the primitive streak, and cells fated to become the epidermis to the periphery. The prospective epidermis at early stages is characterized by the expression of the homeobox gene DLX5, which remains an epidermal marker during gastrulation and neurulation. Later, some DLX5-expressing cells become internalized into the ventral forebrain and the neural crest at the hindbrain level. We studied the mechanism of ectodermal patterning by transplantation of Hensen's nodes and prechordal plates. The DLX5 marker indicates that not only a neural plate, but also a surrounding epidermis is induced in such operations. Similar effects can be obtained with neural plate grafts. These experiments demonstrate that the induction of a DLX5-positive epidermis is triggered by the midline, and the effect is transferred via the neural plate to the periphery. By repeated extirpations of the endoderm we suppressed the formation of an endoderm/mesoderm layer under the epiblast. This led to the generation of epidermis, and to the inhibition of neuroepithelium in the naked ectoderm. This suggests a signal necessary for neural, but inhibitory for epidermal development, normally coming from the lower layers. Finally, we demonstrate that BMP4, as well as BMP2, is capable of inducing epidermal fate by distorting the epidermis-neural plate boundary. This, however, does not happen independently within the neural plate or outside the normal DLX5 domain. In the area opaca, the co-transplantation of a BMP4 bead with a node graft leads to the induction of DLX5, thus indicating the cooperation of two factors. We conclude that ectodermal patterning is achieved by signalling both from the midline and from the periphery, within the upper but also from the lower layers.

The role of retinoid-binding proteins in the generation of pattern in the developing limb, the regenerating limb and the nervous system

Development ◽  
1989 ◽  
Vol 107 (Supplement) ◽  
pp. 109-119 ◽  
Author(s):  
M. Maden ◽  
D. E. Ong ◽  
D. Summerbell ◽  
F. Chytil
Keyword(s):  
Nervous System ◽  
Retinoic Acid ◽  
Chick Embryo ◽  
Neural Tube ◽  
Floor Plate ◽  
Limb Bud ◽  
Commissural Axons ◽  
New Information ◽  
Mantle Layer ◽  
Developing Nervous System

We summarise existing data and describe new information on the levels and distribution of cellular retinoic acid-binding protein (CRABP) and cellular retinolbinding protein (CRBP) in the regenerating axolotl limb, the developing chick limb bud and the nervous system of the chick embryo in the light of the known morphogenetic effects of retinoids on these systems. In the regenerating limb, levels of CRABP rise 3- to 4-fold during regeneration, peaking at the time when retinoic acid (RA) is most effective at causing pattern duplications. The levels of CRBP are low. The potency of various retinoids in causing pattern respecification correlates well with the ability of these compounds to bind to CRABP. In the chick limb bud, the levels of CRABP are high and the levels of CRBP are low. Again the binding of various retinoids to CRABP correlates well with their ability to cause pattern duplications. By immunocytochemistry, we show that CRABP is present at high levels in the progress zone of the limb bud and is distributed across the anteroposterior axis in a gradient with the high point at the anterior margin. In the chick embryo, CRABP levels are high and CRBP levels are low. By immunocytochemistry, CRABP is localised primarily to the developing nervous system, labelling cells and axons in the mantle layer of the neural tube. These become the neurons of the commissural system. Also sensory axons label intensely with CRABP whereas motor axons do not and in the mixed nerves at the brachial plexus sensory and motor components can be distinguished on this basis. In the neural tube, CRBP only stains the ventral floor plate. Since the ventral floor plate may be a source of chemoattractant for commissural axons, we suggest on the basis of these staining patterns that RA may fulfill this role and thus be involved morphogenetically in the developing nervous system.

Early stages of synaptogenesis in the cervical spinal cord of the chick embryo

1973 ◽  
Vol 138 (4) ◽  
pp. 475-488 ◽  
Author(s):  
D. J. Stelzner ◽  
A. H. Martin ◽  
G. L. Scott
Keyword(s):  
Spinal Cord ◽  
Chick Embryo ◽  
Cervical Spinal Cord ◽  
Early Stages

scholarly journals Zinc, vanadate and selenate inhibit the tri-iodothyronine-induced expression of fatty acid synthase and malic enzyme in chick-embryo hepatocytes in culture

1994 ◽  
Vol 303 (1) ◽  
pp. 213-216 ◽  
Author(s):  
Y Zhu ◽  
A G Goodridge ◽  
S R Stapleton
Keyword(s):  
Fatty Acid ◽  
Chick Embryo ◽  
Malic Enzyme ◽  
Fatty Acid Synthase ◽  
Insulin Signalling ◽  
Mrna Levels ◽  
Maximal Inhibition ◽  
Induced Expression ◽  
Expression Of Genes ◽  
Insulin Signalling Pathway

Insulin regulates the expression of genes involved in a variety of metabolic processes. In chick-embryo hepatocytes in culture, insulin amplifies the tri-iodothyronine (T3)-induced enzyme activity, and the level and rate of transcription of mRNA for both fatty acid synthase (FAS) and malic enzyme (ME). Insulin alone, however, has little or no effect on the expression of these genes. In chick-embryo hepatocytes, the mechanism by which insulin regulates the expression of these or other genes is not known. Several recent studies have compared the effects of zinc, vanadate and selenate on insulin-sensitive processes in an attempt to probe the mechanism of insulin action. Because zinc, vanadate and selenate mimic the effects of insulin on several processes, they have been termed insulin-mimetics. We have studied the effect of zinc, vanadate and selenate on the T3-induced expression of both FAS and ME. Like insulin, these agents had little or no effect on the basal activities for FAS and ME in chick-embryo hepatocytes in culture for 48 h. Unlike insulin, however, zinc, vanadate and selenate inhibited the T3-induced activities and mRNA levels of both FAS and ME. Maximal inhibition was achieved at concentrations of 50 microM zinc or vanadate, or 20 microM selenate. Zinc and vanadate also inhibited the T3-induced transcription of the FAS and ME genes. Although the mechanism of this inhibition is unknown, our results indicate that it is not mediated through inhibition of binding of T3 to its nuclear receptor nor through a general toxic effect. Thus zinc, vanadate and selenate are not insulin-mimetics under all conditions, and their effects on other insulin-sensitive processes may be fortuitous and unrelated to actions or components of the insulin signalling pathway.

scholarly journals EXPERIMENTAL STREPTOBACILLUS MONILIFORMIS ARTHRITIS IN THE CHICK EMBRYO

1944 ◽  
Vol 80 (1) ◽  
pp. 59-64 ◽  
Author(s):  
G. John Buddingh
Keyword(s):  
Chick Embryo ◽  
Blood Stream ◽  
Intracellular Parasite ◽  
Synovial Lining ◽  
Infectious Process ◽  
Early Stages ◽  
Streptobacillus Moniliformis ◽  
Rat Bite Fever ◽  
Synovial Lining Cells

1. A strain of Streptobacillus moniliformis isolated from a case of rat bite fever in man has been found to produce infection of the developing chick embryo following inoculation of the chorio-allantois. 2. The disease in embryos is characterized by invasion of the blood stream and an almost exclusive localization of the infectious process to the synovial lining of the joints. 3. In the early stages of the development of the joint lesions the Streptobacillus moniliformis behaves as a facultative intracellular parasite within the cytoplasm of the synovial lining cells. Conditions favorable for the growth of the microorganisms are maintained only temporarily. The infection appears to be self-limiting in nature.

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