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Results for “Embryonic Induction”

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PubMed1992

Cell signals allow the expression of a pre-existent neural pattern in C. elegans.

In C. elegans, a simple pattern develops within a row of epidermal precursor cells, V1-V6. One cell, V5, gives rise to a neuroblast called the postdeirid neuroblast, while the other V cells produce epidermal cells instead. Here we describe experiments suggesting that in order for V5 to produce the postdeirid it must be in close or direct contact with neighboring V cells. Signaling between V cells is required for the formation of the neuroblast; however, which of the V cells can make a postdeirid is not determined by these signals but rather by the action of the homeotic lin-22 and pal-1 genes. These genes prevent V cells in specific body regions from responding to intercellular signals and producing postdeirids. This is a clear example of cell signals playing a permissive rather than an instructive role in neuroblast induction.

Animals↗
PubMed1981

Timed study of experimental primary neural induction.

Experimental primary neural induction was studied by transmission electron microscopy and compared with normal primary neural induction studies. A change was observed in the ectoderm cytoplasm and the ribosomes formed polysomes in the same way as previously described in normal induction.

Animals↗
PubMedDate not supplied

Neural induction.

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Amphibians↗
PubMed1989

Induction of murine 8-cell blastomere polarity by F9 embryonal carcinoma cells.

The individual blastomeres of the preimplantation mouse embryo become polarized during the 8-cell stage of development. This polarity forms as a result of a specific cell-cell interaction that has been termed induction. The ability of embryonal carcinoma (EC) cells to induce 8-cell blastomere polarization has been investigated by aggregating nonpolar 8-cell blastomeres with various types of EC cells. F9, a nullipotent stem cell, induced polarization of a nonpolar 8-cell companion in 80% of the aggregates. Stimulation of differentiation of F9 cells with retinoic acid (RA), with or without dibutyryl cAMP, caused a reduction in the polarity-inducing ability of these cells. Other EC cells, PSA-1, NULLI-SCC1, 3TDM, C3HNE, and P10, all displayed less polarity-inducing activity than F9. In addition, it was observed that when any of these cell types assumed a more differentiated phenotype, either spontaneously or in response to specific stimuli, they displayed a decrease in their ability to induce 8-cell polarization. As a control, the inducing ability of cells from normal mouse tissues was examined. It was found that neither STO mouse fibroblasts nor primary cultures of mouse lymphocytes were able to induce significant polarization of 8-cell stage blastomeres. These data support the hypothesis that while undifferentiated stem cell populations retain the ability to induce 8-cell blastomere polarization, it is apparently lost upon cellular differentiation.

Animals↗
PubMed2006

Induction of midbrain dopaminergic neurons from primate embryonic stem cells by coculture with sertoli cells.

The aim of this study was to produce dopaminergic neurons from primate embryonic stem (ES) cells following coculture with mouse Sertoli cells. After 3 weeks of induction, immunostaining revealed that 90% +/- 9% of the colonies contained tyrosine hydroxylase-positive (TH(+)) neurons, and 60% +/- 7% of the tubulin beta III-positive (Tuj III(+)) neurons were TH(+). Reverse transcription-polymerase chain reaction analyses showed that Sertoli-induced neurons expressed midbrain dopaminergic neuron markers, including TH, dopamine transporter, aromatic amino acid decarboxylase (AADC), receptors such as TrkB and TrkC, and transcription factors NurrI and Lmx1b. Neurons that had been differentiated on Sertoli cells were positive for Pax2, En1, and AADC, midbrain-related markers, and negative for dopamine-beta-hydroxylase, a marker of noradrenergic neurons. These Sertoli cell-induced dopaminergic cells can release dopamine when depolarized by high K(+). Sertoli cell-conditioned medium contained glial cell line-derived neurotrophic factor (GDNF) and supported neuronal differentiation. After pretreatment with anti-GDNF antibody, the percentage of Tuj III(+) colonies was reduced to 14%. Thus, GDNF contributed significantly to inducing primate ES cells into dopaminergic neurons. When transplanted into a 6-hydroxydopamine-treated Parkinson's disease model, primate-derived dopaminergic neurons integrated into the mouse striatum. Two weeks after transplantation, surviving TH(+) cells were present. These TH(+) cells survived for 2 months. Therefore, the induction method of coculture ES cells with Sertoli cells provides an unlimited source of primate cells for the study of pathogenesis and transplantation in Parkinson's disease.

Animals↗
PubMed2001

Cell interactions underlying notochord induction and formation in the chick embryo.

The development of the notochord in the chick is traditionally associated with Hensen's node (the avian equivalent of the organizer). However, recent evidence has shown that two areas outside the node (called the inducer and responder) are capable of interacting after ablation of Hensen's node to form a notochord. It was not clear from these studies what effect (if any) signals from these areas had on normal notochord formation. A third area, the postnodal region, may also contribute to notochord formation, although this has also been questioned. Using transection and grafting experiments, we have evaluated the timing and cellular interactions involved in notochord induction and formation in the chick embryo. Our results indicate that the rostral primitive streak, including the node, is not required for formation of the notochord in rostral blastoderm isolates transected at stages 3a/b. In addition, neither the postnodal region nor the inducer is required for the induction and formation of the most rostral notochordal cells. However, inclusion of the inducer results in considerable elongation of the notochord in this experimental paradigm. Our results also demonstrate that the responder per se is not required for notochord formation, provided that at least the inducer and postnodal region are present, although in the absence of the responder, formation of the notochord occurs far less frequently. We also show that the node is not specified to form notochord until stage 4 and concomitant with this, the inducer loses its ability to induce notochord from the responder. The coincident timing of these changes in the node and inducer suggests that notochord specification and the activity of the inducer are regulated through a negative feedback loop. We propose a model relating our results to the induction of head and trunk organizer activity in the node.

Animals↗
PubMed1999

Analysis of the origin and development of hatching gland cells by transplantation of the embryonic shield in the fish, Oryzias latipes.

Hatching gland cells of the medaka, Oryzias latipes, have been observed to differentiate from the anterior end of the hypoblast, which seems to first involute at the onset of gastrulation. These results suggest that the hatching gland cells of medaka originate from the embryonic shield, the putative organizer of this fish. The present study investigated whether hatching gland cells really originate from the embryonic shield in the medaka. Transplantation experiments with embryonic shield and in situ hybridization detection of hatching enzyme gene expression as a sign of terminal differentiation of the gland cells were carried out. The analysis was performed according to the following processes. First, identification and functional characterization of the embryonic shield region were made by determining the expression of medaka goosecoid gene and its organizer activity. Second, it was confirmed that the embryonic shield had an organizer activity, inducing a secondary embryo, and that the developmental patterns of hatching gland cells in primary and secondary embryos were identical. Finally, the hatching gland cells as identified by hatching enzyme gene expression were found to coincide with the dye-labeled progeny cells of the transplanted embryonic shield. In conclusion, it was determined that hatching gland cells were derived from the embryonic shield that functioned as the organizer in medaka.

Animals↗
PubMed2000

Sequential activation of transcription factors in lens induction.

Since the pioneering work of the early 1900s, the lens has been used as a model system for the study of tissue development in vertebrates. A number of embryological transplantation experiments designed to elucidate the role of tissue interactions in the formation of the lens have led to the proposal of a stepwise determination model. This model has recently been refined through the identification of certain transcription factor genes, which exhibit distinct expression patterns and functional properties in the lens cell lineage. Otx2, Pax6, and Lens1 are induced by the adjacent anterior neural plate and expressed in predifferentiated lens ectoderm. Contact between the optic vesicle and lens ectoderm promotes expression of mafs, Soxs, and Prox1, which are responsible for the initiation of lens differentiation programs including crystallin expression, cell elongation, and cell cycle arrest. Further analysis of the expression and functional characteristics of these transcription factors will allow greater detail when describing the orchestration of genetic programs, which control tissue development from induction to maturation.

Animals↗
PubMed2003

Digital development and morphogenesis.

Signalling interactions between the polarizing region, which produces SHH, and the apical ectodermal ridge, which produces FGFs, are essential for outgrowth and patterning of vertebrate limbs. However, mechanisms that mediate translation of early positional information of cells into anatomy remain largely unknown. In particular, the molecular and cellular basis of digit morphogenesis are not fully understood, either in terms of the formation of the different digits along the antero-posterior axis or in the way digits stop growing once pattern formation has been completed. Here we will review recent data about digit development. Manipulation of morphogenetic signals during digit formation, including application of SHH interdigitally, has shown that digit primordia possess a certain plasticity, and that digit anatomy becomes irreversibly fixed during morphogenesis. The process of generation of joints and thus segmentation and formation of digit tips is also discussed.

Animals↗
PubMed1991

Changes in neural and lens competence in Xenopus ectoderm: evidence for an autonomous developmental timer.

The ability of a tissue to respond to induction, termed its competence, is often critical in determining both the timing of inductive interactions and the extent of induced tissue. We have examined the lens-forming competence of Xenopus embryonic ectoderm by transplanting it into the presumptive lens region of open neural plate stage embryos. We find that early gastrula ectoderm has little lens-forming competence, but instead forms neural tissue, despite its location outside the neural plate; we believe that the transplants are being neuralized by a signal originating in the host neural plate. This neural competence is not localized to a particular region within the ectoderm since both dorsal and ventral portions of early gastrula ectoderm show the same response. As ectoderm is taken from gastrulae of increasing age, its neural competence is gradually lost, while lens competence appears and then rapidly disappears during later gastrula stages. To determine whether these developmental changes in competence result from tissue interactions during gastrulation, or are due to autonomous changes within the ectoderm itself, ectoderm was removed from early gastrulae and cultured for various periods of time before transplantation. The loss of neural competence, and the gain and loss of lens competence, all occur in ectoderm cultured in vitro with approximately the same time course as seen in ectoderm in vitro. Thus, at least from the beginning of gastrulation onwards, changes in competence occur autonomously within ectoderm. We propose that there is a developmental timing mechanism in embryonic ectoderm that specifies a sequence of competences solely on the basis of the age of the ectoderm.

Animals↗