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At least 1,333 records · Page 74Linked to original sources
PubMed1991

Expression of c-kit encoded at the W locus of mice in developing embryonic germ cells and presumptive melanoblasts.

The W locus of mice encodes the c-kit tyrosine kinase receptor. In embryos homozygous for severe W mutations, the number of germ cells does not increase after 8 days of development, melanocytes do not appear, and production of erythrocytes and mast cells is deficient. To gain some insight into the role of the c-kit receptor, we have used in situ hybridization to explore the time period of expression of c-kit transcripts in early germ cells and melanoblasts. At 6 1/2 days of development, expression was not seen in the embryonic cylinder, but did appear in parietal endoderm. Germ cells displayed a low level of c-kit transcripts from their first appearance in the 7 1/2 -day embryo, continuing through early proliferation and migration to the gonad. During migration, surrounding tissues also expressed c-kit. Expression increased in gonia and then ceased as they became nonproliferative. Expression in presumptive melanoblasts was first seen in the cervical region of 10-day embryos and continued as they spread over the surface of the body, entered the epidermis, and differentiated in hair follicles after birth. The effects of mutations of c-kit on germ cells and melanoblasts can be interpreted as an absence of a proliferative signal shortly after their segregation from other cell types. This signal may be required throughout the proliferative phase of early germ cells [and also in postnatal stages of germ cell development (Manova et al. (1990). Development 110, 1057-1069]. In melanoblasts, c-kit may play a role during both proliferation and differentiation.

Animals↗
PubMed1998

The mouse Gtl2 gene is differentially expressed during embryonic development, encodes multiple alternatively spliced transcripts, and may act as an RNA.

We have isolated a novel mouse gene (Gtl2) from the site of a gene trap integration (Gtl2lacZ) that gave rise to developmentally regulated lacZ expression, and a dominant parental-origin-dependent phenotype. Heterozygous Gtl2lacZ mice that inherited the transgene from the father showed a proportionate dwarfism phenotype, whereas the penetrance and expressivity of the phenotype was strongly reduced in Gtl2lacZ mice that inherited the transgene from the mother. Gtl2 expression is highly similar to the beta-galactosidase staining pattern, and is down-regulated but not abolished in mice carrying the Gtl2lacZ insertion. In early postimplantation embryos, Gtl2 is expressed in the visceral yolk sac and embryonic ectoderm. During subsequent development and organogenesis, Gtl2 transcripts are abundant in the paraxial mesoderm closely correlated with myogenic differentiation, in parts of the central nervous system, and in the epithelial ducts of developing excretory organs. The Gtl2 gene gives rise to various differentially spliced transcripts, which contain multiple small open reading frames (ORF). However, none of the ATG codons of these ORFs is in the context of a strong Kozak consensus sequence for initiation of translation, suggesting that Gtl2 might function as an RNA. Nuclear Gtl2 RNA was detected in a temporally and spatially regulated manner, and partially processed Gtl2 transcripts were readily detected in Northern blot hybridizations of polyadenylated RNA, suggesting that primary Gtl2 transcripts are differently processed in various cell types during development. Gtl2 transcript levels are present in parthenogenic embryos but may be reduced, consistent with the pattern of inheritance of the Gtl2lacZ phenotype.

Alternative Splicing↗
PubMed1996

Embryonic development and pattern formation.

During embryogenesis, information encoded in the genome is translated into cell proliferation, morphogenesis, and early stages of differentiation. Embryonic pattern arises from the spatial and temporal regulation and coordination of these events. The vitamin A (retinol) derivative retinoic acid (RA) is essential for normal development. Mammalian embryos are protected against vitamin A deficiency by maternal retinoid homeostasis until stored retinoids fall to very low levels. Retinol binding protein, which is synthesized in the yolk sac placenta of rodent embryos and in the syncytiotrophoblast of the human placenta, is essential for access of retinol to the embryo. Synthesis and metabolism of RA may involve cytoplasmic binding proteins, but the observation that mutants lacking these proteins are normal or near-normal suggests that they are not essential. Severe congenital vitamin A deficiency results in a spectrum of malformations including defects of the eye, lungs, cardiovascular system, and urogenital system. Extreme deficiency results as well in forelimb abnormalities and cleft face, but the embryos are not viable. Similar abnormalities are observed in embryos lacking two retinoid receptors, but loss of one receptor results in either normal development or mild abnormalities. Two single-receptor null mutants, RARgamma-/- and RXRalpha-/-, show regional pattern-specific resistance to teratogenic levels of RA. Mutations leading to abnormality of the structure or regulation of RA signaling pathway genes may be an important cause of human congenital abnormality.

Abnormalities, Multiple↗
PubMed2005

Disruption of insulin-like growth factor-II imprinting during embryonic development rescues the dwarf phenotype of mice null for pregnancy-associated plasma protein-A.

Pregnancy-associated plasma protein-A (PAPP-A), an insulin-like growth factor-binding protein (IGFBP) protease, increases insulin-like growth factor (IGF) activity through cleavage of inhibitory IGFBP-4 and the consequent release of IGF peptide for receptor activation. Mice homozygous for targeted disruption of the PAPP-A gene are born as proportional dwarfs and exhibit retarded bone ossification during fetal development. Phenotype and in vitro data support a model in which decreased IGF-II bioavailability during embryogenesis results in growth retardation and reduction in overall body size. To test the hypothesis that an increase in IGF-II during embryogenesis would overcome the growth deficiencies, PAPP-A-null mice were crossed with DeltaH19 mutant mice, which have increased IGF-II expression and fetal overgrowth due to disruption of IgfII imprinting. DeltaH19 mutant mice were 126% and PAPP-A-null mice were 74% the size of controls at birth. These size differences were evident at embryonic day 16.5. Importantly, double mutants were indistinguishable from controls both in terms of size and skeletal development. Body size programmed during embryo development persisted post-natally. Thus, disruption of IgfII imprinting and consequent elevation in IGF-II during fetal development was associated with rescue of the dwarf phenotype and ossification defects of PAPP-A-null mice. These data provide strong genetic evidence that PAPP-A plays an essential role in determining IGF-II bioavailability for optimal fetal growth and development.

Animals↗
PubMed1998

Disruption of the retinal basal lamina during early embryonic development leads to a retraction of vitreal end feet, an increased number of ganglion cells, and aberrant axonal outgrowth.

Bacterial collagenase was injected into the vitreous of the eye of chick and quail embryos. Immunocytochemical and ultrastructural studies revealed that the collagenase dissolved the retinal basal lamina of the injected eye. The basal lamina disruption was first detectable 1 hour after enzyme injection and was complete within 3 hours. With further development, the retinal basal lamina was not reestablished; newly developing neuroepithelium in the peripheral retina, however, generated an intact basal lamina. Western blot analysis showed that Clostridial collagenase degraded various collagens but spared noncollagenous proteins. Basal lamina disruption of embryonic day 3 to 6 retinae led to the retraction of the end feet of the neuroepithelial cells, caused an increase in the number of Islet-1+ cells (most likely ganglion cells), an increase in the thickness of the optic fiber layer, and aberrant growth of optic axons on their way toward the optic disc. None of these changes were observed when retinal basal laminae were disrupted at later stages of development. The present data demonstrate that the retinal basal lamina, by anchoring the neuroepithelial cells to the pial surface of the retina, has an important function in the development of the normal cytoarchitecture of this structure. It is proposed that the altered extracellular environment in the vitreal part of the retina, resulting in the retraction of the neuroepithelial end feet, is responsible for the increased number of Islet-1+ cells and the aberrant axonal navigation.

Animals↗
PubMed1983

The embryonic development of the cerebellum in normal and reeler mutant mice.

The development of the cerebellum has been studied in normal and reeler mice, from embryonic day fourteen, i.e. when morphogenesis begins in this organ, to birth. The cerebellar nuclei develop according to a similar sequence in both genotypes. Their neurons migrate into the rostral field of the cerebellar bud where they condense in a rounded mass, well defined at E14. From E17, this cell contingent spreads transversally and the three roof nuclei become clearly defined. In reeler mutants, there seems to be an abnormal development of the architectonics of the lateral nucleus. The Purkinje cells migrate into the cortex at the same time in both genotypes. In the normal animal, from E14 onward, Purkinje cells are condensed in a clearly defined plate, where they assume a radial organization. By contrast, the mutant Purkinje cells are not arranged in a plate but are scattered in the periphery of the cortex. The neurons of the external granular layer are identical in both genotypes. Radial glial fibers and early Golgi epithelial cells appear to be normally present in the reeler embryo. The foliation of the cerebellar cortex begins at E17 in the normal embryo. From this stage onward, foliation is increasingly deficient in reeler mutants. Based on these observations, it is suggested that, in normal cerebellar development, a specific, genetically determined mechanism is responsible for the organization and the stabilization of postmigratory neurons and that this mechanism is affected by the reeler mutation.

Animals↗
PubMed2003

Histological studies on embryonic development of the rabbit heart.

Two experiments were performed to evaluate the normal development of the rabbit heart. In the first experiment the most intensive period of heart development was determined in rabbit embryos. The second experiment studied the most intensive period of heart development, determined in the first experiment, by concentrated sampling at 8-hour intervals. After cutting open the uterine wall opposite the discoid placenta, rabbit embryos were removed from the ampullae of the uterus using capillary tubes, under stereomicroscope at fivefold magnification. The embryos were subsequently placed into 4% formalin solution for 24 h. After fixation, slides stained with haematoxylin and eosin were made for histological examination. In the first experiment 51 embryos were examined, while during the second experiment a total of 113 embryos, representing different stages of development, were collected. Finally the data obtained on rabbits were compared with the well-known development of the heart in humans and mice.

Animals↗
PubMed2003

Immunohistochemical analysis of protein gene product 9.5, a ubiquitin carboxyl-terminal hydrolase, during placental and embryonic development in the mouse.

Protein gene product 9.5 (PGP9.5) is expressed at high level in the neural and neuroendocrine systems. We investigated the localization and degree of expression of PGP9.5 in the developing mouse placenta and embryo at 6.5, 10.5 and 14 days of gestation using an immunohistochemical technique. At 6.5 days of gestation PGP9.5 was detected at various levels in decidual and primary trophoblast giant cells in the placenta, and in embryonic ectodermal cells in the embryo. At 10.5 and 14 days of gestation PGP9.5 was expressed at moderate to strong levels in neurons in the embryo, but rarely in the placenta. These findings suggest that the protein may play a significant role in implantation and placental development, and differentiation of embryonic ectoderm.

Animals↗
PubMed1997

Dystroglycan is essential for early embryonic development: disruption of Reichert's membrane in Dag1-null mice.

Dystroglycan is a central component of the dystrophin-glycoprotein complex (DGC), a protein assembly that plays a critical role in a variety of muscular dystrophies. In order to better understand the function of dystroglycan in development and disease, we have generated a null allele of dystroglycan (Dag1neo2) in mice. Heterozygous Dag1neo2 mice are viable and fertile. In contrast, homozygous Dag1neo2 embryos exhibit gross developmental abnormalities beginning around 6.5 days of gestation. Analysis of the mutant phenotype indicates that an early defect in the development of homozygous Dag1neo2 embryos is a disruption of Reichert's membrane, an extra-embryonic basement membrane. Consistent with the functional defects observed in Reichert's membrane, dystroglycan protein is localized in apposition to this structure in normal egg cylinder stage embryos. We also show that the localization of two critical structural elements of Reichert's membrane--laminin and collagen IV--are specifically disrupted in the homozygous Dag1neo2 embryos. Taken together, the data indicate that dystroglycan is required for the development of Reichert's membrane. Furthermore, these results suggest that disruption of basement membrane organization might be a common feature of muscular dystrophies linked to the DGC.

Amino Acid Sequence↗