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PubMed1996

Transcription of the beta 1 tubulin (beta Tub56D) gene in apodemes is strictly dependent on muscle insertion during embryogenesis in Drosophila melanogaster.

The insertion of the somatic musculature into the epidermis during embryogenesis of Drosophila melanogaster represents an excellent system for the investigation of cell-cell communication processes. Evidence from earlier experiments suggested that the expression of the beta 1 tubulin gene from D. melanogaster in the epidermal attachments may be dependent upon myotube insertion. Analysis of the transcription of the beta 1 tubulin gene in mutants for pair-rule or segment polarity genes revealed strong coupling of the induction process to myotube insertion. Involvement of extracellular matrix proteins of the integrin family could be excluded since beta 1 mRNA is detectable in the apodemes in mutants for the common subunit PS beta until muscles detach late in embryogenesis. Furthermore, the lack of specific muscles in the myogenic mutants rolling stone (rost) and not enough muscles (nem) eliminates beta 1 transcription exclusively in the corresponding apodemes. The data presented clearly show that the transcription of the beta 1 tubulin gene in the muscle attachment sites is activated by myotube insertion by a yet unidentified pathway.

Animals↗

PubMed1997

Expression of syndecan-1 and -3 during embryogenesis of the central nervous system in relation to binding with midkine.

Midkine (MK) is a 13-kDa heparin-binding growth/differentiation factor, and its interaction with heparan sulfate proteoglycan is important in promotion of neurite outgrowth. This study was performed to reveal the species of syndecans that interact with MK during embryogenesis of the central nervous system in the rat. Northern blot analysis and immunohistochemical staining using antibodies to syndecans showed that syndecan-1 was strongly expressed in the brain and spinal cord of the 10-day rat fetus, and the expression became weak as embryogenesis proceeded. On the other hand, syndecan-3 expression was stronger both in the brain and spinal cord in the later developmental period (day 14-16 of gestation). No significant expression of ryudocan (syndecan-4) was detected in fetal brains by Northern blot analysis. Syndecan-3 isolated from 16-day rat fetus bound to MK strongly, as did syndecan-1 isolated from 10-day rat fetus. Thus, both syndecan-1 and syndecan-3 were considered to be involved in interaction with MK during construction of the central nervous system; syndecan-1 is expected to play important roles in the earlier periods, and syndecan-3 in the later periods.

Animals↗

PubMedDate not supplied

Multiple phases of expression and regulation of mouse Hoxc8 during early embryogenesis.

Hox genes are expressed in dynamic patterns during embryogenesis consistent with their role in axial specifications. To study the distribution of mouse Hoxc8, a homeodomain containing protein, we raised monoclonal antibodies against the least conserved portion of Hoxc8. Using these antibodies, we have examined early and mid-gestation embryos for the distribution of the protein. At the end of gastrulation Hoxc8 is expressed in the caudal portion of the embryo. In the neural tube, an early phase when all cells express Hoxc8 is distinguished from a late phase with predominant expression in differentiating neurons. A comparison of this expression pattern with that of a reporter gene under the control of the early Hoxc8 enhancer demarcates three separate regulatory components: (1) initiation and establishment; (2) maintenance; and (3) downregulation. We propose that Hoxc8 expression during embryogenesis is established in multiple phases. Possible regulatory mechanisms involved in generating such a complex domain of Hox gene expression are discussed.

Animals↗

PubMed2000

Imprinted H19 gene expression in embryogenesis and human cancer: the oncofetal connection.

Cancer cells resemble embryonal cells morphologically and share with them characteristics such as reduced differentiation, rapid proliferation rate, and increased motility. Genes expressed in embryogenesis, down-regulated with tissue maturation and reexpressed in cancer, are designated as oncofetal genes, and many of them are used as tumor markers. The H19 gene is an imprinted gene that is expressed from the maternal allele and functions as an RNA molecule. It is abundantly expressed in fetal life and down-regulated postnatally. We have shown oncofetal expression of H19 in human cancer. The study of H19 expression in testicular germ cell tumors of adolescents and young adults, which follow lines of differentiation of the conceptus, demonstrates dissociation between level of expression and monoallelic versus biallelic expression, which are two independent oncofetal characteristics of cancer. Expression of the maternally expressed H19 from the paternal allele in the villous cytotrophoblastic cells of the androgenetic complete hydatidiform mole is designated relaxation of imprinting. H19 is abundantly expressed in the fetal bladder mucosa and in carcinoma of the urinary bladder. It is a marker of early recurrence and may be used as a potential basis for gene therapy.

Alleles↗

PubMed1997

Embryogenesis of the phrenic nerve and diaphragm in the fetal rat.

The embryogenesis of the mammalian phrenic nerve and diaphragm continues to be poorly understood. The purpose of this study was to reexamine this general issue and resolve some long-standing controversies. Specifically, we examined 1) the migratory path and the initial target for phrenic axons; 2) the relationship between the phrenic nerve and the primordial diaphragm during descent from the cervical to the thoracic spinal cord levels; and 3) the nature of the interaction between the progression of phrenic nerve intramuscular branching, myoblast and/or myogenic cell migration, and diaphragmatic myotube formation. We demonstrate that a leading group of "pioneering" phrenic axons migrate along a well-defined track of neural cell adhesion molecule (NCAM)-expressing and low-affinity nerve growth factor (p75) receptor-expressing cells to reach the primordial diaphragm, the pleuroperitoneal fold, at embryonic day (E) 13. During the next day of development, the phrenic nerve and the primordial diaphragm descend together toward the level of the thoracic spinal cord. By E14.5, intramuscular branching has commenced. There is a tight spatiotemporal correlation between the outgrowth of intramuscular phrenic nerve branches, the distribution of myoblasts and/or myogenic cells, and the formation of myotubes within the developing diaphragm, implicating intimate mutual regulation.

Animals↗

PubMed1997

Expression patterns of the four nuclear factor I genes during mouse embryogenesis indicate a potential role in development.

The nuclear factor I (NFI) family of site-specific DNA-binding proteins is required for both the cell-type specific transcription of many viral and cellular genes and for the replication of adenovirus DNA. Although binding sites for NFI proteins within the promoters of several tissue-specific genes have been shown to be essential for their expression, it is unclear which NFI gene products function in specific tissues during development. We have isolated cDNAs from all four murine NFI genes (gene designations Nfia, Nfib, Nfic, and Nfix), assessed the embryonic and postnatal expression patterns of the NFI genes, and determined the ability of specific NFI proteins to activate transcription from the NFI-dependent mouse mammary tumor virus (MMTV) promoter. In adult mice, all four NFI genes are most highly expressed in lung, liver, heart, and other tissues but only weakly expressed in spleen and testis. The embryonic expression patterns of the NFI genes is complex, with NFI-A transcripts appearing earliest-within 9 days postcoitum in the heart and developing brain. The four genes exhibit unique but overlapping patterns of expression during embryonic development, with high level expression of NFI-A, NFI-B, and NFI-X transcripts in neocortex and extensive expression of the four genes in muscle, connective tissue, liver, and other organ systems. The four NFI gene products studied differ in their ability to activate expression of the NFI-dependent MMTV promoter, with the NFI-B protein being most active and the NFI-A protein being least active. These data are discussed in the context of the developmental expression patterns of known NFI-responsive genes. The differential activation of an NFI-dependent promoter, together with the expression patterns observed for the four genes, indicate that the NFI proteins may play an important role in regulating tissue-specific gene expression during mammalian embryogenesis.

Amino Acid Sequence↗

PubMed1997

Developmental expression of perlecan during murine embryogenesis.

Perlecan is a modular heparan sulfate proteoglycan that is an intrinsic constituent of all basement membranes and extracellular matrices. Because of its strategic position and unique structure, perlecan has been implicated in modulating the activity of various growth factors required for normal development and tissue homeostasis. To gain insights into the potential function of perlecan in vivo, we examined the spatiotemporal distribution of its mRNA and protein core during murine embryogenesis. We utilized a new affinity-purified antibody that recognizes specifically the protein core of perlecan together with an in situ RT-PCR approach to perform a systematic analysis of perlecan expression and deposition during murine ontogeny. Perlecan appeared early (E10.5) in tissues of vasculogenesis including heart, pericardium, and major blood vessels. Its early expression coincided with the development of the cardiovascular system. Subsequently (E11-13), the greatest deposition of perlecan occurred within the developing cartilage, especially the cartilage undergoing endochondral ossification, where it remained elevated throughout all the developmental stages, and up to adulthood. Interestingly, the mRNA levels of perlecan were always higher in all the vascularized tissues, principally within endothelial cells, while chondrocytes displayed relatively low mRNA levels. This suggests a higher biosynthesis and turnover rates in the blood vessels vis-à-vis those of cartilaginous and other mesenchymal tissues. During later stages of development (E13-17.5) perlecan mRNA levels progressively increased and its expression correlated with the onset of tissue differentiation of various parenchymal organs including the developing kidneys, lungs, liver, spleen, and gastrointestinal tract. The central nervous system showed no perlecan expression with the exception of the calvaria and choroid plexus. Collectively, the results indicate that perlecan may play crucial roles not only in vasculogenesis but also in the maturation and maintenance of differentiated tissues, including cartilage.

Animals↗

PubMed1998

Chicken winged-helix transcription factor cFKH-1 prefigures axial and appendicular skeletal structures during chicken embryogenesis.

The cDNA cFKH-1 encodes a chicken winged helix/forkhead domain transcription factor that presents a dynamic expression pattern during chicken embryogenesis. Transcripts accumulate predominantly in early paraxial mesoderm, developing somites, and within mesenchymal precursors of skeletal structures. cFKH-1 RNA is first detected in the developing mesoderm of HH stage 6 embryos. During subsequent development cFKH-1 RNA accumulates in a dorsal domain of the anterior presomitic mesoderm and later in all cells of the epithelial somites before it becomes limited to the sclerotome when somites compartmentalise. cFKH-1 expression persists in the sclerotome, forming the vertebrae and in mesenchymal condensations in limb buds that will give rise later to the appendicular bones. In differentiated chondrocytes and definitive bone structures, however, cFKH-1 expression is down-regulated. Additional expression domains are found in mesenchyme of branchial arches and the head, in the dorsal aorta, and weakly in the endocardium. Based on its expression pattern and the structure of the forkhead DNA-binding domain cFKH-1 constitutes a chicken relative to the murine family of fkh-1/MF1 and MFH-1 factors. The embryonic expression of the cFKH-1 gene defines distinct mesodermal domains and suggests that it may regulate gene expression in mesenchymal cell lineages that will form cartilage in trunk and limb buds.

Amino Acid Sequence↗

PubMed1999

Zebrafish stat3 is expressed in restricted tissues during embryogenesis and stat1 rescues cytokine signaling in a STAT1-deficient human cell line.

Transcription factors of the STAT family are required for cellular responses to multiple signaling molecules. After ligand binding-induced activation of cognate receptors, STAT proteins are phosphorylated, hetero- or homodimerize, and translocate to the nucleus. Subsequent STAT binding to specific DNA elements in the promoters of signal-responsive genes alters the transcriptional activity of these loci. STAT function has been implicated in the transduction of signals for growth, reproduction, viral defense, and immune regulation. We have isolated and characterized two STAT homologs from the zebrafish Danio rerio. The stat3 gene is expressed in a tissue-restricted manner during embryogenesis, and larval development with highest levels of transcript are detected in the anterior hypoblast, eyes, cranial sensory ganglia, gut, pharyngeal arches, cranial motor nuclei, and lateral line system. In contrast, the stat1 gene is not expressed during early development. The stat3 gene maps to a chromosomal position syntenic with the mouse and human STAT3 homologs, whereas the stat1 gene does not. Despite a higher rate of evolutionary change in stat1 relative to stat3, the stat1 protein rescues interferon-signaling functions in a STAT1-deficient human cell line, indicating that cytokine-signaling mechanisms are likely to be conserved between fish and tetrapods. Dev Dyn 1999;215:352-370.

Amino Acid Sequence↗

PubMed1999

Two novel sites of expression of NADPH cytochrome P450 reductase during murine embryogenesis: limb mesenchyme and developing olfactory neuroepithelia.

While all cells in eukaryotic organisms probably express the gene encoding NADPH cytochrome P450 reductase, we identified two novel sites which have the highest local concentrations of P450 reductase transcripts during murine embryogenesis. One site is in developing limbs, including lateral limb bud mesenchyme and condensing mesenchyme in the footplate which will form precartilage. A second site is in primitive neuroepithelia, including future olfactory epithelia and olfactory lobes of the brain. These high, local concentrations of P450 reductase transcripts revealed by in situ hybridization were transient and most prominent between embryonic (E) days 12.5-15.5. They cannot be explained by the known functions for P450 reductase. The precursor nature of the highest reductase-expressing cells suggests that differentiation-specific mechanisms regulate P450 reductase gene transcription during organogenesis. The data suggest this multifunctional protein might serve an important role in the formation of precartilage models from condensing limb mesenchyme and in the early development of joints that will form at apposed surfaces of these models.

Animals↗

PubMed2000

Spatiotemporal expression patterns of mammalian chordin during postgastrulation embryogenesis and in postnatal brain.

Chordin is an antagonist of TGFbeta-like bone morphogenetic proteins (BMPs) that plays roles in dorsoventral axis formation and in induction, maintenance and/or differentiation of neural tissue in early vertebrate embryogenesis. In contrast, little is known concerning possible roles for Chordin at later stages of vertebrate development and in the adult. To provide insights into possible postgastrulation roles for Chordin, we report the spatiotemporal expression patterns of Chordin in 8.5- to 15.5-dpc mouse embryos and in the postnatal mouse brain. Expression of Chordin in the primordia of most major organs from 10.5 dpc, including the brain, lung, heart, liver, kidney, thymus, and gut, suggests multiple functions for Chordin in organogenesis, potentially by means of interactions with TGFbeta-like BMPs. The relatively high levels of Chordin expression in condensing and differentiating cartilage elements from 11.5 dpc indicates a generalized role for Chordin throughout embryonic skeletogenesis. In the postnatal mouse brain, we demonstrate that Chordin is coexpressed with other components of the TGFbeta-like BMP signalling pathway in the cerebellum and hippocampus, sites of high synaptic plasticity, suggesting a role for Chordin in this process.

Animals↗

PubMed1998

Embryogenesis of tracheal atresia.

A spectrum of tracheo-esophageal anomalies has been described in an adriamycin-treated model with common features to the human pattern. Tracheal agenesis was part of this spectrum. It is a rare congenital anomaly that has not been described in embryos. Virgin timed-pregnant Sprague-Dawley rats were injected with adriamycin i.p. at a dose of 2 mg/Kg on days 6-9 of gestation (plug day = day 0). Fetuses were recovered at term and histologic assessment of tracheo-esophageal anomalies was made. Also, embryos were removed on different gestational days and the embryology of these defects was analysed. Two out of sixty-two fetuses and nine out of 180 embryos were identified with tracheal atresia. Type III tracheal atresia was seen in the full-term fetuses with a tracheo-esophageal fistula arising from the origin of the left main bronchus. Day 13 embryos did not show normal tracheal development; instead, the lung buds developed from the ventral aspect of the foregut which continued to the stomach as a lower esophageal segment. A blind ending pouch was seen on the ventral aspect of the upper part of the foregut. The embryogenesis of tracheal atresia was similar to that of esophageal atresia except that the blind upper foregut pouch developed ventrally rather than dorsally.

Abnormalities, Drug-Induced↗

PubMed1999

Shaw-like potassium currents in the auditory rhombencephalon throughout embryogenesis.

The Shaw subfamily of potassium channel genes, including Kv3.1, are highly expressed within the auditory nuclei of the brainstem, where they have been implicated in the characteristic response properties of particular types of neurons. Potassium currents carried by Kv3.1 are voltage-dependent, have a high activation threshold, are slow to inactivate, and are very sensitive to 4-aminopyridine (4-AP) and tetraethylammonium (TEA). We have investigated the developmental appearance of potassium currents in cell cultures from nucleus magnocellularis and its precursor neuroblasts from the acoustico-vestibular anlage of the chicken. Whole-cell patch recordings revealed that high-threshold, sustained, outward currents were present in 91% of neuroblasts. These currents displayed high sensitivities to TEA and 4-AP. The remaining 9% of neuroblasts exhibited only transient outward currents. Most cells (74%) had both a sustained and an initial transient component of outward current. These current types were observed throughout embryogenesis, beginning with the earliest ages (embryonic day [E]2). During proliferation and migration, and early neuronal differentiation, current levels were low; they incremented gradually during the time when the first synapses occur on dendrites and increased 2- to 3-fold just before hatching, when axosomatic synapses form. These findings suggest that the Shaw subfamily of channels in nucleus magnocellularis may be involved in early neuronal development, as well as in synaptic function later on.

4-Aminopyridine↗

PubMed1996

Changes in nuclear localization of An3, a RNA helicase, during oogenesis and embryogenesis in Xenopus laevis.

The immunolocalization of An3 protein, an ATP-dependent RNA helicase and a member of the DEAD box family, was compared with the localization of fibrillarin, a protein essential for rRNA processing, and snRNPs, which are involved in mRNA splicing reactions, during oogenesis and embryogenesis in Xenopus laevis. Although An3 protein was detected in the cytoplasm of all stages of oocytes, in most stages An3 protein was also present in the nucleus. Prior to stage I An3 protein was uniformly dispersed throughout the entire germinal vesicle; from stages I to V it was in nucleoli. By stage VI nucleolar labeling with anti-An3 disappeared and the protein was no longer present within nuclei. An3 reactivity was also present throughout the nuclei of follicle cells surrounding prestage I to stage VI oocytes. Both cytoplasmic and nuclear An3 staining were present in cells of stages 8 to 35 embryos; however, nuclear staining was punctate and uniformly distributed throughout the nucleoplasm. Fibrillarin was diffusely distributed throughout the entire germinal vesicle prior to stage I, localized exclusively to nucleoli of oocytes between stages I and VI and in nucleoli of stages 12 and 35 embryonic cells. Reactivity for snRNPs (anti-Sm) in germinal vesicles of prestage I oocytes was diffuse, and similar to the distribution of An3 and fibrillarin; in later stage oocytes anti-Sm staining was restricted to a population of granules, much fewer in number and more heterogeneous in size than nucleoli. Anti-Sm activity was apparent in nuclei of embryonic cells of stages 8 to 35 embryos. Although colocalization of the Sm epitope and An3 was not observed in developing oocytes and in embryonic cells, Sm reactive material was frequently found in close association with An3-positive nucleoli (oocytes) and nuclear deposits (embryonic cells). In stage IV and V oocytes treated with actinomycin D (4 micrograms/ml) to inhibit rRNA synthesis, nucleoli, which continued to possess fibrillarin, lacked An3; staining of follicle cell nuclei for An3 was unchanged. Treatment with 200 micrograms/ml actinomycin D to block mRNA synthesis, inhibited An3 but not fibrillarin staining in nuclei of prestage I oocytes and follicle cells. The changing patterns of An3 reactivity and the differential effects of actinomycin D on such localizations observed here are consistent with a role for An3 in the processing/production of RNA.

Animals↗

PubMed1998

Selective loss of mouse embryos due to the expression of transgenic major histocompatibility class I molecules early in embryogenesis.

Among the numerous hypotheses proposed to explain the absence of fetal rejection by the mother in mammals, it has been suggested that regulation of expression of the polymorphic major histocompatibility complex (MHC) at the fetal-maternal interface plays a major role. In addition to a lack of MHC gene expression in the placenta throughout gestation, the absence of polymorphic MHC molecules on the early embryo, as well as their low level of expression after midgestation, could contribute to this important biologic phenomenon. In order to test this hypothesis, we have produced transgenic mice able to express polymorphic MHC class I molecules early in embryogenesis. We have placed the MHC class la gene H-2Kb under the control of a housekeeping gene promoter, the hydroxy-methyl-glutaryl coenzyme A reductase (HMG) gene minimal promoter. This construct has been tested for functionality after transfection into mouse fibroblast L cells. The analysis of three founder transgenic mice and their progeny suggested that fetoplacental units that could express the H-2Kb heavy chains are unable to survive in utero beyond midgestation. We have shown further that a much higher resorption rate, on days 11 to 13 of embryonic development, is observed among transgenic embryos developing from eggs microinjected at the one-cell stage with the pHMG-Kb construct than in control embryos. This lethality is not due to immune phenomena, since it is observed in histocompatible combinations between mother and fetus. These results are discussed in the context of what is currently known about the regulation of MHC expression at the fetal-maternal interface and in various transgenic mouse models.

Animals↗

PubMed1996

Co-expression of the HGF/SF and c-met genes during early mouse embryogenesis precedes reciprocal expression in adjacent tissues during organogenesis.

Early experiments with cells in culture and recent targeting experiments have confirmed that the mesenchyme-derived growth factor hepatocyte growth factor/scatter factor (HGF/SF) is a paracrine agent that regulates the development of several epithelial and myogenic precursor cells during organogenesis. Here, we report the expression pattern of HGF/SF and its receptor, the product of the proto-oncogene c-met, during gastrulation and early organogenesis in mouse embryo. During gastrulation, the expression of HGF/SF and c-met overlaps. Initially the two genes are expressed in the endoderm and in the mesoderm along the rostro-intermediate part of the primitive streak and, later, in the node and in the notochord. Neither HGF/SF nor c-met is expressed in the ectodermal layer throughout gastrulation. During early organogenesis, overlapping expression of HGF/SF and c-met is found in heart, condensing somites and neural crest cells. However, a second and distinct pattern of expression, characterized by the presence of the ligand in mesenchymal tissues and the receptor in the surrounding ectoderm, is seen in the bronchial arches and in the limb buds. At 13 days postcoitum (d.p.c.), only this second pattern of expression is observed in differentiated somites and several major organs (i.e., lungs, liver, and gut). The expression of the HGF/SF and c-met genes throughout embryogenesis suggests a shift from an autocrine to a paracrine signaling system. The shift takes place in early organogenesis and implies different roles of HGF/SF in development. During gastrulation, HGF/SF may affect the fate of migrating mesodermal cells and may play a role in axis determination, whereas during organogenesis, the expression patterns of HGF/SF and its receptor reflect the recently established roles in the growth of certain epithelia and the migration of specific myogenic precursor cells.

Animals↗

PubMed2000

Targeted insertion of a lacZ reporter gene into the mouse Cer1 locus reveals complex and dynamic expression during embryogenesis.

The mouse Cer1 (mCer1, Cer-l, Cerr1) gene encodes one member of a family of cytokines structurally and functionally related to the Xenopus head-inducing factor, Cerberus (xCer). We generated a mouse line in which the Cer1 gene was inactivated by replacing the first coding exon with a lacZ reporter gene. Mice homozygous for this allele (Cer1(lacZ)) showed no apparent perturbation of embryogenesis or later development. However, the lacZ reporter revealed a number of hitherto uncharacterised sites of Cer1 expression in late fetal and adult tissues. Preliminary analysis suggests that Cer1 is not essential for their morphogenesis, differentiation, or homeostasis.

Animals↗

PubMed2000

alpha(1)-Adrenergic stimulation perturbs the left-right asymmetric expression pattern of nodal during rat embryogenesis.

BACKGROUND: Normal development of the left/right (L/R) body axis leads to the characteristic sidedness of asymmetric body structures, e.g., the left-sided heart. Several genes are now known to be expressed with L/R asymmetry during embryogenesis, including nodal, a member of the transforming growth factor-beta (TGF-beta) family. Mutations or experimental treatments that affect L/R development, such as those that cause situs inversus (reversal of the sidedness of asymmetric body structures), have been shown to alter or abolish nodal's asymmetric expression. METHODS: In the present study, we examined the effects on nodal expression of alpha(1)-adrenergic stimulation, known to cause a 50% incidence of situs inversus in rat embryos grown in culture, using reverse transcription-polymerase chain reaction assay and whole-mount in situ hybridization assay. RESULTS: In embryos cultured with phenylephrine, an alpha(1)-adrenergic agonist, nodal's normal asymmetric expression only in the left lateral plate mesoderm was altered. In some treated embryos, nodal expression was detected in either the left or right lateral plate mesoderm. However, most treated embryos lacked lateral plate mesoderm expression. In addition, the embryos that did show expression were at a later stage than when nodal expression is normally found. CONCLUSIONS: Our results demonstrate that alpha(1)-adrenergic stimulation delays the onset and perturbs the normal asymmetric pattern of nodal expression. Either of these effects might contribute to situs inversus.

Adrenergic alpha-Agonists↗