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PubMed1977

Biochemical investigation of lens induction in vitro. I. Induction properties of the eye cup and ectodermal response.

1. Optic cups of 48, 72 and 96 hours old chick embryos were prepared, cultured and recombined with ectoderm. With the optic cups of 48 hours old embryos, lens formation occurred in 16% of the cases. With the optic cups of 72 hours old embryos, lens formation occurred in 28% of the cases. Optic cups of 96 hours old embryos were not able to induce a lens. 2. The optic cup proved to be able to induce a lens more than once. 3. Ectoderm of the head of 72 hours old embryos was still able to form a lens. 4. Using homogenized eye cups of 72 hours old embryos, lens induction occurred only in a few cases. When the optic cups were cut into small pieces, lens induction occurred in 30% of the cases. This suggests that intact cells are necessary to obtain lens induction.

Animals↗
PubMed2002

Induction and patterning of the cardiac conduction system.

The cardiac conduction system (CCS) is the component of the heart that initiates and maintains a rhythmic heartbeat. As the embryonic heart forms, the CCS must continue to develop and mature in a coordinated manner to ensure that proper pace making potential and distribution of action potential is maintained at all stages. This requires not only the formation of distinct and disparate components of the CCS, but the integration of these components into a functioning whole as the heart matures. Though research in this area of development may have lagged behind other areas of heart development, in recent years there has been much progress in understanding the ontogeny of the CCS and the developmental cues that drive its formation. This is largely due to studies on the avian heart as well as the use of molecular biology approaches. This review gives a perspective on advances in understanding the development of the vertebrate CCS, and reports new data illuminating the mechanism of conduction cell determination and maintenance in the mammalian heart. As much of our knowledge about the development of the CCS has been derived from the chick embryo, one important area facing the field is the relationship and similarities between the structure and development of avian and mammalian conduction systems. Specifically, the morphology of the distal elements of the mammalian CCS and the manner in which its components are recruited from working cardiomyocytes are areas of research that will, hopefully, receive more attention in the near future. A more general and outstanding question is how the disparate components of all vertebrate conduction systems integrate into a functional entity during embryogenesis. There is mounting evidence linking the patterning and formation of the CCS to instructive cues derived from the cardiac vasculature and, more specifically, to hemodynamic-responsive factors produced by cardiac endothelia. This highlights the need for a greater understanding of the biophysical forces acting on, and created by, the cardiovascular system during embryonic development. A better understanding of these processes will be necessary if therapeutics are to be developed that allow the regeneration of damaged cardiac tissues or the construction of biologically engineered heart tissues.

Animals↗
PubMed1983

Control of tyrosinase gene expression and its relationship to neural crest induction in Rana pipiens. I. Isolation and characterization of amphibian tyrosinase mRNA.

Rana pipiens tyrosinase mRNA was isolated from Stage 22 (tailfin circulation) embryos by indirect immunoprecipitation of embryonic polysomes using highly specific rabbit anti-tyrosinase and goat-(anti-rabbit) immunoglobulins. Analysis on sucrose gradients indicated that anti-tyrosinase bound specifically to embryonic polysomes of the 300-350 S class coincident with the location of nascent tyrosinase enzyme activity and tyrosinase mRNA. These same anti-tyrosinase-bound polysomes were fully immunoprecipitated by the addition of goat-(anti-rabbit) IgG. Poly(A+) RNA was obtained from phenol-extracted antibody. polysome complexes by sequential passage over oligo(dT)-cellulose. The final purification of tyrosinase mRNA was achieved by preparative sucrose gradient fractionation. Tyrosinase mRNA sedimented as a single 13 S peak in 5-30% sucrose gradients and tracked on sodium dodecyl sulfate-polyacrylamide gels as a single band of 4.5 X 10(5) Da (1275 nucleotides). When assayed in a cell-free translation system, this mRNA directed the synthesis of a single 35,000-Da protein which co-migrated with native tyrosinase on sodium dodecyl sulfate-polyacrylamide gels and which was greater than 98% immunoprecipitable by anti-tyrosinase immunoglobulin. Final purification was 4103-fold over the starting polysomal RNA.

Animals↗
PubMed1994

Combinatorial signaling in development.

Intercellular signaling plays a major role in the development of vertebrate and invertebrate embryos. In several cases, including the induction of mesoderm and neural ectoderm induction in Xenopus and the induction of the vulva in C. elegans, multiple intercellular signals are utilized. This review examines a number of examples of signaling in development wherein two signals combine to affect the fate of a cell. The examples are placed in distinct categories, based on whether the signals synergize with or antagonize one another, and on the inductive potential of the individual signals. These types of combinatorial signaling events are suggested to be a general feature of embryonic development.

Animals↗
PubMed2002

Antimorphic PV.1 causes secondary axis by inducing ectopic organizer.

Xenopus homeobox gene, PV.1 ventralizes activin-induced dorsal mesoderm and inhibits neuralization of ectoderm in animal cap when overexpressed. Here we generated PV.1/engrailed fusion construct (N-PV1-EnR) to perform loss-of-function study for this transcription factor. N-PV1-EnR showed an extremely antimorphic effect, causing a partial secondary embryonic axis when expressed at ventral marginal zone of blastula. In ventral marginal zone cells, this chimeric protein induced organizer genes and suppressed ventral markers mimicking those effects reported for dominant negative BMP-4 receptor (DNBR). Moreover, N-PV1-EnR rescued the ventralized embryos caused by the ectopic dorsal expression of PV.1 but not by that of Xvent-2. These results suggested that PV.1 functions at downstream of BMP-4 as a ventralizing effector which acts separately from Xvent-2 and the dominant negative effect gained by this specific mutant is applicable for the further studies of BMP-4 downstream pathway.

Activin Receptors, Type I↗
PubMed2001

Patterning mechanisms controlling vertebrate limb development.

Vertebrate limb buds are embryonic structures for which much molecular and cellular data are known regarding the mechanisms that control pattern formation during development. Specialized regions of the developing limb bud, such as the zone of polarizing activity (ZPA), the apical ectodermal ridge (AER), and the non-ridge ectoderm, direct and coordinate the development of the limb bud along the anterior-posterior (AP), dorsal-ventral (DV), and proximal-distal (PD) axes, giving rise to a stereotyped pattern of elements well conserved among tetrapods. In recent years, specific gene functions have been shown to mediate the organizing and patterning activities of the ZPA, the AER, and the non-ridge ectoderm. The analysis of these gene functions has revealed the existence of complex interactions between signaling pathways operated by secreted factors of the HH, TGF-beta/BMP, WNT, and FGF superfamilies, which interact with many other genetic networks to control limb positioning, outgrowth, and patterning. The study of limb development has helped to establish paradigms for the analysis of pattern formation in many other embryonic structures and organs.

Animals↗
PubMed1995

Role of MAP kinase in mesoderm induction and axial patterning during Xenopus development.

We have examined the role of MAP kinase during mesoderm induction and axial patterning in Xenopus embryos. MAP Kinase Phosphatase (MKP-1) was used to inactivate endogenous MAP kinase and was found to prevent the induction of early and late mesodermal markers by both FGF and activin. In whole embryos, MKP-1 was found to disrupt posterior axial patterning, generating a phenotype similar to that obtained with a dominant inhibitory FGF receptor. Overexpression of either constitutively active MAP kinase or constitutively active MAP kinase (MEK) was sufficient to induce Xbra expression, while only constitutively active MEK was able to significantly induce expression of muscle actin. When MAP kinase phosphorylation was used as a sensitive marker of FGF receptor activity in vivo, this activity was found to persist at a low and relatively uniform level throughout blastula stage embryos. The finding that a low level of MAP kinase phosphorylation exists in unstimulated animal caps and is absent in caps overexpressing a dominant inhibitory FGF receptor provides a basis for our previous observation that overexpression of this receptor inhibits activin induction. These results indicate that FGF-dependent MAP kinase activity plays a critical role in establishing the responsiveness of embryonic tissues to mesoderm inducers.

Activins↗
PubMed1996

Induction of connexin 32 expression by potential embryonic signals in rabbit uterine epithelium.

Connexin 32 induction is found in rabbit uterine epithelium as a response to embryo recognition. Here we have chosen this connexin 32 expression as a cell biological marker to define the type of a locally acting embryonic signal. 17 beta-estradiol, onapristone, catechol estrogen (4-hydroxy-estradiol), prostaglandins E2 and F2 alpha, db-cAMP, and glass beads as mechanical stimuli were given to pseudopregnant animals on day 4, 5 or 6 posthuman chorionic gonadotropin (hCG). The induction of connexin 32 corresponded to the time of implantation at days 6-8 post-hCG by immunohistochemistry and Northern blot analysis. Untreated pseudopregnant animals started to express connexin 32 on day 8 post-hCG. In animals treated with 4-hydroxy-estradiol, 17 beta-estradiol or prostaglandins, connexin 32 expression started 1 day earlier (day 7 post-hCG) and led to an enhanced connexin 32 expression on day 8 post-hCG compared to control animals. The antigestagen, onapristone, as well as cAMP did not alter the endogenous program. Mechanical stimuli led to a high expression of connexin 32 starting at day 7 post-hCG whereas in pregnancy the blastocyst induces connexin 32 expression from day 6 postcoitum onwards. Combination of mechanical stimuli with 17 beta-estrogen advanced the induction to day 6 post-hCG. We conclude that a mechanical stimulus in combination with 17 beta-estradiol induces connexin 32 synthesis in a similar manner as compared to the blastocyst during pregnancy.

Animals↗
PubMed1982

Cell contact-dependent regulation of hormonal induction of glutamine synthetase in embryonic neural retina.

Glutamine synthetase (GS) is a differentiation marker in the neural retina of the chick embryo. GS is localized specifically in Müller glia cells, and it can be precociously induced by adrenal corticosteroids (such as cortisol). The induction depends on cortisol-elicited gene expression and results in de novo synthesis of GS and in a multifold increase in its level. GS is inducible only when Müller cells are closely associated with retina neurons. When retina tissue from 10-day embryos is dissociated into single cells and these are maintained either in suspension or in monolayer culture, GS cannot be induced. However, if identically prepared cells are reaggregated and allowed to reconstruct retinotypic associations, they are inducible for GS. Measurements of cytoplasmic cortisol-receptors showed that cell dissociation results in a rapid and marked reduction in the level (or activity) of these receptors. Their low level persists if the cells are maintained in a dispersed state. However, if the cells are reaggregated and reestablish tissue-like contacts, the level of cortisol receptors increases, as does GS inducibility. The results indicate that, in the embryonic neural retina, histotypic cell contacts are involved in regulating the level of cytoplasmic cortisol receptors and of the responsiveness of Müller glia cells to the induction of GS. Whether the two aspects are causally related is a matter for future study.

Animals↗
PubMed1996

Hlx homeo box gene is essential for an inductive tissue interaction that drives expansion of embryonic liver and gut.

The divergent murine homeo box gene Hlx is expressed in restricted hematopoietic cell types and, during embryogenesis, prominently in visceral mesenchyme of the developing liver, gall bladder, and gut. Targeted disruption of the gene has now established that it plays a key role in visceral organogenesis. Embryos homozygous for the mutation died around embryonic day 15 with anemia and severe hypoplasia of the liver and gut. Liver ontogeny commenced normally with formation of the liver diverticulum and differentiation of hepatocytes, but the organ failed to expand and reached only 3% of normal size. The apparent liver hypoplasia was not associated with a notable increase in apoptotic cells. Gut development also began normally, but the intestines failed to undergo extensive elongation and looping and reached only a quarter of normal length. The anemia resulted from a deficiency in the fetal form of hematopoiesis, which occurs in the liver, but no intrinsic defect in Hlx-/- hematopoietic cells was observed in vitro, and liver-derived Hlx-/- hematopoietic stem cells that were transplanted to irradiated normal mice could fully reconstitute hematopoiesis. The impaired fetal hematopoiesis therefore reflects insufficient support function provided by the minute liver. Hlx is normally expressed in visceral mesenchyme lying adjacent to the developing liver and gut epithelia affected by the mutation, but not in the epithelia themselves. Hence, Hlx regulates a mesenchymal-epithelial interaction that drives a vital growth phase in visceral organogenesis. Moreover, because mutation of Hlx blocked liver growth but not its specification, early morphogenesis, or differentiation, development of this organ appears to occur by step-wise inductive interactions under separate genetic control.

Animals↗
PubMed1998

Inhibition of mesoderm formation by follistatin.

Mesoderm induction requires interaction between cells of the animal and vegetal hemispheres of the embryo. Several molecules have been proposed as candidates for mesoderm-inducing signals, with activin a particularly strong candidate. However, it has not been possible to inhibit mesoderm formation in vivo by specifically blocking activin action. Follistatin is able to inhibit the action of activin but not that of the mature region of Vg1, a member of the transforming growth factor beta family. Follistatin therefore provides a useful tool for distinguishing between signalling by these two factors. We have overexpressed Xenopus follistatin mRNA and analysed the expression of several mesodermal markers. Our results show an inhibition of mesodermal formation by follistatin in a concentration-dependent manner, showing the requirement of activin for mesodermal induction.

Animals↗