The origin and movements of the hepatogenic cells in the chick embryo as determined by radioautographic mapping

Development ◽  
1971 ◽  
Vol 25 (1) ◽  
pp. 97-113
Author(s):  
Glenn C. Rosenquist
Keyword(s):  
Chick Embryo ◽  
Developmental Stage ◽  
Primitive Streak ◽  
Limb Bud ◽  
Chick Embryos ◽  
Lateral Plate Mesoderm ◽  
Lateral Plate ◽  
Somite Stage ◽  
Definition Of ◽  
Exact Definition

The origin of the prehepatic cells was determined by tracing the movements of [3H]thymidine-labelled grafts excised from medium-streak to 4-somite stage chick embryos and transplanted to the epiblast, streak and endoderm-mesoderm layer of similarly staged recipient embryos. Although exact definition of prehepatic areas was not possible because of the small number of grafts placed at each developmental stage, the study showed in general that at the medium-streak stage, the prehepatic endoderm cells are in the anterior third of the primitive streak; they shortly begin to migrate anteriorly and laterally into the endoderm layer ventral to the precardiac areas of mesoderm. They are in the yolk-sac endoderm at the 2–4-somite stage, and by the 15–17-somite stage are clustered at the anterior intestinal portal. At the 26-somite to early limb-bud stages, the anterior and posterior liver diverticula have formed from these endoderm cells, and some of the branches of the diverticula may have reached the prehepatic mesenchyme, where the two tissues have begun to form cords and sinuses. At the medium-streak stage, the prehepatic mesoderm is located slightly more than halfway from the anterior to the posterior end of the primitive streak. From this position it migrates anteriorly and laterally into the lateral plate mesoderm, and from the head-process to the 2–4-somite stage it is situated posterior to the prehepatic endoderm and posterior and lateral to the heart-forming portion of the splanchnic layer. By the 15–17-somite stage the prehepatic mesoderm has reached a position in the splanchnic layer of mesoderm which forms the dorsolateral wall of the sinus venosus. By the 26-somite to early limb-bud stage the hepatic diverticula have joined with the hepatic mesenchyme to form the rudimentary cords and sinuses of the liver.

The origin and movement of the limb-bud epithelium and mesenchyme in the chick embryo as determined by radioautographic mapping

Development ◽  
1971 ◽  
Vol 25 (1) ◽  
pp. 85-96
Author(s):  
Glenn C. Rosenquist
Keyword(s):  
Primitive Streak ◽  
Limb Bud ◽  
Lateral Margin ◽  
Lateral Plate ◽  
Posterior Limb ◽  
Process Stage ◽  
The Future ◽  
Dorsal Portion ◽  
Definition Of ◽  
Area Pellucida

The origin of the limb-bud cells was determined by tracing the movements of [3H]thymidine-labelled grafts excised from late medium-streak to 5-somite stage chick embryos and transplanted to the epiblast, streak, and endoderm-mesoderm of similarly staged recipient embryos. Although exact definition of the prelimb areas was not possible because of the small number of grafts placed at each developmental stage, the study showed in general that at the late medium-streak stage the future limb-bud epithelium is in the epiblast (dorsal) layer near the lateral margin of the area pellucida. It moves medially toward the embryonic axis, just lateral to the premesoderm cells which will be invaginated at the primitive streak. With regression of the streak, the limb-bud epithelium moves relatively anteriorly into a position dorsal to the limb-bud mesoderm, beginning at least as early as the early head-fold stage. At the definitive-streak stage, the future limb-bud mesoderm is in the epiblast layer about halfway from the streak to the lateral margin of the area pellucida, at a level about halfway between the anterior and posterior ends of the streak. From this position the prelimb mesoderm migrates medially to the streak, and is invaginated into the mesoderm layer at a position about halfway between the anterior and posterior ends of the streak; after the head-process stage, it migrates anteriorly and laterally into the somatic layer of the lateral plate, ventral to the limb-bud epithelium. Mesoderm which will form the anterior limb-bud migrates anterior to mesoderm which will form the posterior limb-bud; mesoderm which will form the ventral portion of each limb-bud migrates posterolateral to mesoderm which will form the dorsal portion of each limb-bud.

The origin and movement of prelung cells in the chick embryo as determined by radioautographic mapping

Development ◽  
1970 ◽  
Vol 24 (3) ◽  
pp. 497-509
Author(s):  
Glenn C. Rosenquist
Keyword(s):  
Chick Embryo ◽  
Primitive Streak ◽  
Lateral Margin ◽  
Chick Embryos ◽  
Process Stage ◽  
Somite Stage ◽  
Dorsal Mesentery ◽  
Area Pellucida

The origin of the prelung cells was determined by tracing the movements of [3H]thymidinelabelled grafts excised from medium-streak to 4-somite stage chick embryos and transplanted to the epiblast, streak, and endoderm-mesoderm of similarly staged recipient embryos. At the medium-streak stage the prelung endoderm cells are in the anterior third of the primitive streak; they shortly begin to migrate anteriorly and laterally into the endoderm layer. They are folded into the gut beginning at about the 4-somite stage, and begin to reach their definitive position in the ventrolateral gut wall at the 10- to 16-somite stage. At the ± 22-somite stage the prelung endoderm begins to burrow into the overlying splanchnic layer of mesoderm, pushing the prelung mesoderm ahead of it. At the medium-streak stage the prelung mesoderm is in the epiblast (dorsal) layer about half-way to the lateral margin of the area pellucida on either side of the streak, at a level about half-way between the anterior and posterior ends of the streak. From this position the prelung mesoderm migrates medially to the streak and is invaginated into the mesoderm layer at a position about half-way between the anterior and posterior ends of the streak. As a section of the dorsal mesentery, it migrates anteriorly and laterally from the streak into the splanchnic mesoderm lateral to the somites. From the head process stage to the early somite stages, the prelung mesoderm is located posterior to the prelung endoderm. The prelung mesoderm continues to migrate with the splanchnic mesoderm into the mesentery dorsal to the heart, where it invests the prelung endoderm after the 16- to 19-somite stage. Beginning at about the 22-somite stage, the prelung endoderm penetrates the prelung mesoderm and the bilateral bronchi are formed.

Extracellular matrix synthesis in the chick embryo lateral plate prior to and during limb outgrowth

Development ◽  
1980 ◽  
Vol 59 (1) ◽  
pp. 71-87
Author(s):  
Trent D. Stephens ◽  
N. S. Vasan ◽  
James W. Lash
Keyword(s):  
Extracellular Matrix ◽  
Chick Embryo ◽  
Molecular Basis ◽  
Limb Bud ◽  
Matrix Synthesis ◽  
Lateral Plate ◽  
Limb Buds ◽  
Cartilage Development ◽  
Limb Outgrowth ◽  
Lateral Plates

Little is known at the present time about the molecular basis and mechanisms of morphogenesis. The present study is an attempt to determine what influence the extracellular matrix has on the initial outgrowth of the limb bud. Stage -12 to -18 chick embryo lateral plates were examined in relation to proline and sulfate incorporation into collagen and proteoglycan. The flank and limbs incorporated the same amount of labeled proline and sulfate before stage 16. At stage 16 the flank began to incorporate more of both isotopes until at stage 18 there was twice as much incorporation into the flank as into the limbs. The flank and limbs contained the same type of collagen during the period examined. The limbs contained both large and small proteoglycans but the flank contained only small proteoglycans. These data suggest that the extracellular matrix in the flank and limb regions may play a role in limb outgrowth and that the limb buds at these stages may be more inclined toward cartilage development.

The mesenchymal factor, FGF10, initiates and maintains the outgrowth of the chick limb bud through interaction with FGF8, an apical ectodermal factor

Development ◽  
1997 ◽  
Vol 124 (11) ◽  
pp. 2235-2244 ◽  
Author(s):  
H. Ohuchi ◽  
T. Nakagawa ◽  
A. Yamamoto ◽  
A. Araga ◽  
T. Ohata ◽  
...  
Keyword(s):  
Sonic Hedgehog ◽  
Limb Bud ◽  
Fibroblast Growth ◽  
Lateral Plate Mesoderm ◽  
Lateral Plate ◽  
Bud Formation ◽  
Limb Mesenchyme ◽  
Vertebrate Limb ◽  
Fgf10 Expression ◽  
Zone Of Polarizing Activity

Vertebrate limb formation has been known to be initiated by a factor(s) secreted from the lateral plate mesoderm. In this report, we provide evidence that a member of the fibroblast growth factor (FGF) family, FGF10, emanates from the prospective limb mesoderm to serve as an endogenous initiator for limb bud formation. Fgf10 expression in the prospective limb mesenchyme precedes Fgf8 expression in the nascent apical ectoderm. Ectopic application of FGF10 to the chick embryonic flank can induce Fgf8 expression in the adjacent ectoderm, resulting in the formation of an additional complete limb. Expression of Fgf10 persists in the mesenchyme of the established limb bud and appears to interact with Fgf8 in the apical ectoderm and Sonic hedgehog in the zone of polarizing activity. These results suggest that FGF10 is a key mesenchymal factor involved in the initial budding as well as the continuous outgrowth of vertebrate limbs.

Hox-4 gene expression in mouse/chicken heterospecific grafts of signalling regions to limb buds reveals similarities in patterning mechanisms

Development ◽  
1992 ◽  
Vol 115 (2) ◽  
pp. 553-560 ◽  
Author(s):  
J.C. Izpisua-Belmonte ◽  
J.M. Brown ◽  
A. Crawley ◽  
D. Duboule ◽  
C. Tickle
Keyword(s):  
Gene Expression ◽  
Gene Network ◽  
Primitive Streak ◽  
Mouse Embryos ◽  
Limb Bud ◽  
Chick Embryos ◽  
Mouse Limb ◽  
Mouse Cells ◽  
Species Specific ◽  
Genital Tubercle

The products of Hox-4 genes appear to encode position in developing vertebrate limbs. In chick embryos, a number of different signalling regions when grafted to wing buds lead to duplicated digit patterns. We grafted tissue from the equivalent regions in mouse embryos to chick wing buds and assayed expression of Hox-4 genes in both the mouse cells in the grafts and in the chick cells in the responding limb bud using species specific probes. Tissue from the mouse limb polarizing region and anterior primitive streak respecify anterior chick limb bud cells to give posterior structures and lead to activation of all the genes in the complex. Mouse neural tube and genital tubercle grafts, which give much less extensive changes in pattern, do not activate 5′-located Hox-4 genes. Analysis of expression of Hox-4 genes in mouse cells in the grafted signalling regions reveals no relationship between expression of these genes and strength of their signalling activity. Endogenous signals in the chick limb bud activate Hox-4 genes in grafts of mouse anterior limb cells when placed posteriorly and in grafts of mouse anterior primitive streak tissue. The activation of the same gene network by different signalling regions points to a similarity in patterning mechanisms along the axes of the vertebrate body.

The forkhead transcription factor Foxf1 is required for differentiation of extra-embryonic and lateral plate mesoderm

Development ◽  
2001 ◽  
Vol 128 (2) ◽  
pp. 155-166 ◽  
Author(s):  
M. Mahlapuu ◽  
M. Ormestad ◽  
S. Enerback ◽  
P. Carlsson
Keyword(s):  
Transcription Factor ◽  
Cell Adhesion ◽  
Posterior Part ◽  
Homeobox Gene ◽  
Primitive Streak ◽  
Yolk Sac ◽  
Lateral Plate Mesoderm ◽  
Forkhead Transcription Factor ◽  
Lateral Plate ◽  
Adhesion Properties

The murine Foxf1 gene encodes a forkhead transcription factor expressed in extra-embryonic and lateral plate mesoderm and later in splanchnic mesenchyme surrounding the gut and its derivatives. We have disrupted Foxf1 and show that mutant embryos die at midgestation due to defects in mesodermal differentiation and cell adhesion. The embryos do not turn and become deformed by the constraints of a small, inflexible amnion. Extra-embryonic structures exhibit a number of differentiation defects: no vasculogenesis occurs in yolk sac or allantois; chorioallantoic fusion fails; the amnion does not expand with the growth of the embryo, but misexpresses vascular and hematopoietic markers. Separation of the bulk of yolk sac mesoderm from the endodermal layer and adherence between mesoderm of yolk sac and amnion, indicate altered cell adhesion properties and enhanced intramesodermal cohesion. A possible cause of this is misexpression of the cell-adhesion protein VCAM1 in Foxf1-deficient extra-embryonic mesoderm, which leads to co-expression of VCAM with its receptor, alpha(4)-integrin. The expression level of Bmp4 is decreased in the posterior part of the embryo proper. Consistent with this, mesodermal proliferation in the primitive streak is reduced and somite formation is retarded. Expression of Foxf1 and the homeobox gene Irx3 defines the splanchnic and somatic mesodermal layers, respectively. In Foxf1-deficient embryos incomplete separation of splanchnic and somatic mesoderm is accompanied by misexpression of Irx3 in the splanchnopleure, which implicates Foxf1 as a repressor of Irx3 and as a factor involved in coelom formation.

An early marker of axial pattern in the chick embryo and its respecification by retinoic acid

Development ◽  
1992 ◽  
Vol 114 (4) ◽  
pp. 841-852 ◽  
Author(s):  
O. Sundin ◽  
G. Eichele
Keyword(s):  
Retinoic Acid ◽  
Chick Embryo ◽  
Protein A ◽  
Ectopic Expression ◽  
Primitive Streak ◽  
Expression Domain ◽  
Lateral Plate ◽  
Antibody Staining ◽  
Discrete Band ◽  
Stage Embryo

Chick Ghox 2.9 protein, a homeodomain-containing polypeptide, is first detected in the mid-gastrula stage embryo and its levels increase rapidly in the late gastrula. At this time, the initially narrow band of expression along the primitive streak expands laterally to form a shield-like domain that encompasses almost the entire posterior region of the embryo and extends anteriorly as far as Hensen's node. We have found that this expression domain co-localizes with a morphological feature that consists of a stratum of refractile, thickened mesoderm. Antibody-staining indicates that Ghox 2.9 protein is present in all cells of this mesodermal region. In contrast, expression within the ectoderm overlying the region of refractile mesoderm varies considerably. The highest levels of expression are found in ectoderm near the streak and surrounding Hensen's node, regions that recent fate mapping studies suggest that primarily destined to give rise to neurectoderm. At the definitive streak stage (Hamburger and Hamilton stage 4) the chick embryo is especially sensitive to the induction of axial malformations by retinoic acid. Four hours after the treatment of definitive streak embryos with a pulse of retinoic acid the expression of Ghox 2.9 protein is greatly elevated. This ectopic expression occurs in tissues anterior to Hensen's node, including floor plate, notochord, presumptive neural plate and lateral plate mesoderm, but does not occur in the anteriormost region of the embryo. The ectopic induction of Ghox 2.9 is strongest in ectoderm, and weaker in the underlying mesoderm. Endoderm throughout the embryo is unresponsive. At stage 11, Ghox 2.9 is normally expressed at high levels within rhombomere 4 of the developing hindbrain. In retinoic-acid-treated embryos which have developed to this stage, typical rhombomere boundaries are largely absent. Nevertheless, Ghox 2.9 is still expressed as a discrete band, but one that is widened and displaced to a more anterior position.

scholarly journals Multi-modal effects of BMP signaling on Nodal expression in the lateral plate mesoderm during left–right axis formation in the chick embryo

2013 ◽  
Vol 374 (1) ◽  
pp. 71-84 ◽  
Author(s):  
Kenjiro Katsu ◽  
Norifumi Tatsumi ◽  
Daisuke Niki ◽  
Ken-ichi Yamamura ◽  
Yuji Yokouchi
Keyword(s):  
Chick Embryo ◽  
Bmp Signaling ◽  
Axis Formation ◽  
Lateral Plate Mesoderm ◽  
Lateral Plate

REGULATION OF THE INITIATION OF HEMOGLOBIN SYNTHESIS IN THE BLOOD ISLAND CELLS OF CHICK EMBRYOS: I. QUALITATIVE STUDIES OF THE EFFECTS OF ACTINOMYCIN AND δ-AMINOLEVULINIC ACID

1966 ◽  
Vol 44 (11) ◽  
pp. 1543-1560 ◽  
Author(s):  
S. D. Wainwright ◽  
Lillian K. Wainwright
Keyword(s):  
Aminolevulinic Acid ◽  
Basal Medium ◽  
Primitive Streak ◽  
Chick Embryos ◽  
Messenger Rnas ◽  
Stages Of Development ◽  
Linear Rate ◽  
Hemoglobin Synthesis ◽  
Naked Eye ◽  
Somite Stage

Intact and de-embryonated blastodiscs of chick embryos from all stages of development between the definitive primitive streak and the 10-somite stage were incubated on simple solid synthetic media. On the basal medium, blastodiscs at all initial stages of development synthesized hemoglobin readily visible to the naked eye within 24 hours, incorporated leucine into protein at an approximately linear rate for 24 hours, and incorporated uridine into RNA at a roughly linear rate for at least 6 hours after a short lag.Blastodiscs taken before the 1-somite stage failed to synthesize any detectable hemoglobin on medium containing 2 μg/ml of actinomycin, whereas those token at later stages synthesized hemoglobin visible to the naked eye. This concentration of actinomycin totally inhibited the incorporation of uridine into high molecular weight RNA within 2–3 hours, but the incorporation of leucine into protein was not inhibited for 6–8 hours. The residual incorporation of uridine was entirely into the soluble RNA fraction.At 10 μg/ml, actinomycin markedly inhibited the synthesis of hemoglobin by blastodiscs taken at stages earlier than the 6-somite embryo, but did not markedly affect hemoglobin synthesis by the more advanced blastodiscs. This concentration of actinomycin caused only slightly greater inhibition of the incorporation of uridine into acid-precipitable material than the smaller concentration for all blastodiscs, and was not markedly more inhibitory for the incorporation of leucine into protein.The presence of δ-aminolevulinic acid overcame the inhibitions of synthesis of hemoglobin by actinomycin but did not prevent the inhibitions of incorporation of uridine into RNA and of leucine into protein.Regulation of the onset of rapid hemoglobin synthesis appears to be at the translation level, probably through the supply of δ-aminolevulinic acid. The latter is probably regulated through synthesis of RNAs formed at the head-fold stage. Messenger RNAs for globin synthesis are present at the stage of the definitive primitive streak.

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