Hepatic induction in the avian embryo: Specificity of reactive endoderm and inductive mesoderm

Mesoderm of precardiac and cardiac region (‘cardiac’ mesoderm) of chick, quail and mouse embryos could induce hepatic epithelium in the endoderm of the anterior half of young quail or chick embryos (anterior endoderm) in vitro as well as in vivo. No species specificity in the induction of hepatic epithelium by the ‘cardiac’ mesoderm could be observed. The hepatic induction, was controlled strictly by tissue specificity of both endoderm and mesoderm. Replacement of the ‘cardiac’ mesoderm or the anterior endoderm by noncardiac mesoderms or endoderms other than the anterior endoderm resulted in failure of hepatic induction. Only the anterior endoderm was found to have competence for hepatic induction, indicating that it was committed, in unknown ways, to react with ‘cardiac’ mesoderm, and can properly be called pre-hepatic endoderm. Comparison between the development of hepatic endoderm and the hepatic induction potency of ‘cardiac’ mesoderm, which was most intense during 1- to 1·5- incubation days and decreased gradually with the increase of the stage, suggests that in normal development the ‘cardiac’ mesoderm actually induces hepatic epithelium in the competent endoderm. Hepaticinduction potency remained up to 6 days, and was found in truncus arteriosus, ventricle and auricle areas and in endocardial and myocardial layers of the heart.

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The Hierarchic Order of Intermediate Filament Structure and Assembly

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100120308 ◽

1985 ◽

Vol 43 ◽

pp. 722-725

Author(s):

U. Aebi ◽

E.C. Glavaris ◽

R. Eichner

Keyword(s):

Tissue Specificity ◽

Structural Model ◽

Eukaryotic Cells ◽

Cdna Sequencing ◽

Filament Structure ◽

Keratin Filaments ◽

Isoelectric Points ◽

Immunological Crossreactivity

Five different classes of intermediate-sized filaments (IFs) have been identified in differentiated eukaryotic cells: vimentin in mesenchymal cells, desmin in muscle cells, neurofilaments in nerve cells, glial filaments in glial cells and keratin filaments in epithelial cells. Despite their tissue specificity, all IFs share several common attributes, including immunological crossreactivity, similar morphology (e.g. about 10 nm diameter - hence ‘10-nm filaments’) and the ability to reassemble in vitro from denatured subunits into filaments virtually indistinguishable from those observed in vivo. Further more, despite their proteinchemical heterogeneity (their MWs range from 40 kDa to 200 kDa and their isoelectric points from about 5 to 8), protein and cDNA sequencing of several IF polypeptides (for refs, see 1,2) have provided the framework for a common structural model of all IF subunits.

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Adhesion molecules during somitogenesis in the avian embryo.

The Journal of Cell Biology ◽

10.1083/jcb.104.5.1361 ◽

1987 ◽

Vol 104 (5) ◽

pp. 1361-1374 ◽

Cited By ~ 182

Author(s):

J L Duband ◽

S Dufour ◽

K Hatta ◽

M Takeichi ◽

G M Edelman ◽

...

Keyword(s):

Adhesion Molecules ◽

Tissue Remodeling ◽

Cell Aggregation ◽

Avian Embryo ◽

Primary Role ◽

Calcium Dependent ◽

Tissue Dissociation ◽

Spatio Temporal

In avian embryos, somites constitute the morphological unit of the metameric pattern. Somites are epithelia formed from a mesenchyme, the segmental plate, and are subsequently reorganized into dermatome, myotome, and sclerotome. In this study, we used somitogenesis as a basis to examine tissue remodeling during early vertebrate morphogenesis. Particular emphasis was put on the distribution and possible complementary roles of adhesion-promoting molecules, neural cell adhesion molecule (N-CAM), N-cadherin, fibronectin, and laminin. Both segmental plate and somitic cells exhibited in vitro calcium-dependent and calcium-independent systems of cell aggregation that could be inhibited respectively by anti-N-cadherin and anti-N-CAM antibodies. In vivo, the spatio-temporal expression of N-cadherin was closely associated with both the formation and local disruption of the somites. In contrast, changes in the prevalence of N-CAM did not strictly accompany the remodeling of the somitic epithelium into dermamyotome and sclerotome. It was also observed that fibronectin and laminin were reorganized secondarily in the extracellular spaces after CAM-mediated contacts were modulated. In an in vitro culture system of somites, N-cadherin was lost on individual cells released from somite explants and was reexpressed when these cells reached confluence and established intercellular contacts. In an assay of tissue dissociation in vitro, antibodies to N-cadherin or medium devoid of calcium strongly and reversibly dissociated explants of segmental plates and somites. Antibodies to N-CAM exhibited a smaller disrupting effect only on segmental plate explants. In contrast, antibodies to fibronectin and laminin did not perturb the cohesion of cells within the explants. These results emphasize the possible role of cell surface modulation of CAMs during the formation and remodeling of some transient embryonic epithelia. It is suggested that N-cadherin plays a major role in the control of tissue remodeling, a process in which N-CAM is also involved but to a lesser extent. The substratum adhesion molecules, fibronectin and laminin, do not appear to play a primary role in the regulation of these processes but may participate in cell positioning and in the stabilization of the epithelial structures.

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Wound healing in chick embryos in vivo and in vitro

Developmental Biology ◽

10.1016/0012-1606(59)90031-4 ◽

1959 ◽

Vol 1 (3) ◽

pp. 302-326 ◽

Cited By ~ 29

Author(s):

Paul Weiss ◽

A.Gedeon Matoltsy

Keyword(s):

Wound Healing ◽

Chick Embryos

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Lethality of a tritiated amino acid in early mouse embryos

Development ◽

10.1242/dev.88.1.209 ◽

1985 ◽

Vol 88 (1) ◽

pp. 209-217

Author(s):

Janet L. Wiebold ◽

Gary B. Anderson

Keyword(s):

Specific Activity ◽

Subsequent Development ◽

Blastocyst Stage ◽

Mouse Embryos ◽

Radiation Induced ◽

Specific Activities ◽

Tritiated Amino Acids ◽

Early Mouse

2- to 4-cell and morula- to blastocyst-stage mouse embryos were cultured for 1 h in tritiated leucine at two specific activities and their subsequent development followed in vitro and in vivo (after transfer to recipients), respectively. 2- to 4-cell embryos that incorporated an average of 42 d.p.m. per embryo were impaired in their ability to develop to the morula and blastocyst stage. Recipients receiving morulae and blastocysts that had incorporated an average of 384 d.p.m. per embryo failed to produce young. Reduction of the specific activity improved the viability of embryos both in vitro and in vivo but development was still less than that of unlabelled embryos. Protein degradation curves were different for both 2- to 4-cell and morulato blastocyst-stage embryos labelled at the two different specific activities. Most studies using tritiated amino acids have employed higher specific activities than those used here and they may have to be reevaluated due to the possibility of radiation-induced artifacts.

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

Development ◽

10.1242/dev.69.1.151 ◽

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.

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Localization of cytoskeletal proteins in preimplantation mouse embryos

Development ◽

10.1242/dev.55.1.211 ◽

1980 ◽

Vol 55 (1) ◽

pp. 211-225

Author(s):

E. Lehtonen ◽

R. A. Badley

Keyword(s):

Blastocyst Stage ◽

Cytoskeletal Proteins ◽

Mouse Embryos ◽

Trophectoderm Cells ◽

Apparent Concentration ◽

Preimplantation Mouse ◽

Early Mouse ◽

Filament Protein

The immunofluorescence technique was used to detect the presence and distribution of actin, alpha-actinin, tubulin and 10 nm filament protein in early mouse embryos. Actin and alpha-actinin stainings showed a distinct concentration to a peripheral layer in the cleavage-stage blastomeres and in trophectoderm cells. Dots of fluorescence appeared in this cortical staining pattern. The distribution of tubulin staining in the blastomere cytoplasm was relatively even with apparent concentration at the perinuclear region and frequently at wide intercellular contact areas. 10 nm filament protein was distributed evenly in the blastomere cytoplasm without cortical concentration of the label. At the blastocyst stage, the trophectoderm cells in blastocyst outgrowths in vitro developed well organized cytoskeletons including both microfilament, microtubule and 10 nm filament elements. Comparable structures were not observed in blastocysts in vivo, or in late hatched blastocysts cultured in suspension. The morphogenetic significance of the observations is discussed.

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Divergent functions and distinct localization of the Notch ligands DLL1 and DLL3 in vivo

The Journal of Cell Biology ◽

10.1083/jcb.200702009 ◽

2007 ◽

Vol 178 (3) ◽

pp. 465-476 ◽

Cited By ~ 84

Author(s):

Insa Geffers ◽

Katrin Serth ◽

Gavin Chapman ◽

Robert Jaekel ◽

Karin Schuster-Gossler ◽

...

Keyword(s):

Golgi Apparatus ◽

Mouse Embryos ◽

Functional Equivalence ◽

Presomitic Mesoderm ◽

Drosophila Wing ◽

Wing Discs ◽

Golgi Network ◽

Notch Ligands

The Notch ligands Dll1 and Dll3 are coexpressed in the presomitic mesoderm of mouse embryos. Despite their coexpression, mutations in Dll1 and Dll3 cause strikingly different defects. To determine if there is any functional equivalence, we replaced Dll1 with Dll3 in mice. Dll3 does not compensate for Dll1; DLL1 activates Notch in Drosophila wing discs, but DLL3 does not. We do not observe evidence for antagonism between DLL1 and DLL3, or repression of Notch activity in mice or Drosophila. In vitro analyses show that differences in various domains of DLL1 and DLL3 individually contribute to their biochemical nonequivalence. In contrast to endogenous DLL1 located on the surface of presomitic mesoderm cells, we find endogenous DLL3 predominantly in the Golgi apparatus. Our data demonstrate distinct in vivo functions for DLL1 and DLL3. They suggest that DLL3 does not antagonize DLL1 in the presomitic mesoderm and warrant further analyses of potential physiological functions of DLL3 in the Golgi network.

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