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PubMed1998

Embryonic lethality and abnormal cardiac myocytes in mice lacking ryanodine receptor type 2.

The ryanodine receptor type 2 (RyR-2) functions as a Ca2+-induced Ca2+ release (CICR) channel on intracellular Ca2+ stores and is distributed in most excitable cells with the exception of skeletal muscle cells. RyR-2 is abundantly expressed in cardiac muscle cells and is thought to mediate Ca2+ release triggered by Ca2+ influx through the voltage-gated Ca2+ channel to constitute the cardiac type of excitation-contraction (E-C) coupling. Here we report on mutant mice lacking RyR-2. The mutant mice died at approximately embryonic day (E) 10 with morphological abnormalities in the heart tube. Prior to embryonic death, large vacuolate sarcoplasmic reticulum (SR) and structurally abnormal mitochondria began to develop in the mutant cardiac myocytes, and the vacuolate SR appeared to contain high concentrations of Ca2+. Fluorometric Ca2+ measurements showed that a Ca2+ transient evoked by caffeine, an activator of RyRs, was abolished in the mutant cardiac myocytes. However, both mutant and control hearts showed spontaneous rhythmic contractions at E9.5. Moreover, treatment with ryanodine, which locks RyR channels in their open state, did not exert a major effect on spontaneous Ca2+ transients in control cardiac myocytes at E9.5-11.5. These results suggest no essential contribution of the RyR-2 to E-C coupling in cardiac myocytes during early embryonic stages. Our results from the mutant mice indicate that the major role of RyR-2 is not in E-C coupling as the CICR channel in embryonic cardiac myocytes but it is absolutely required for cellular Ca2+ homeostasis most probably as a major Ca2+ leak channel to maintain the developing SR.

Animals↗
PubMed2006

2-D DIGE as a quantitative tool for investigating the HUPO Brain Proteome Project mouse series.

Brain development and aging is a complex process involving proliferation, differentiation and apoptosis. Elucidating proteome changes in these processes can help to understand the mechanisms of brain development and maintenance as well as neurodegenerative diseases. The research reported here is a contribution to the HUPO Brain Proteome Project mouse pilot study. Whole, frozen C57BL/6J mouse brain comprising three different developmental stages (embryonic day 16, postnatal day 7, and postnatal days 54-58) were processed by using 2-D DIGE. A total of 1999 spots were matched between all gels. Of these, 206 spots were differentially expressed between the different stages: 122 spots were highest in intensity in embryonic stage E16, 26 highest in the juvenile group P7 and 58 spots highest in P56, the adult stage. The results show a pattern of temporal expression. Based on the expression patterns we tentatively suggest that proteins involved in the establishment of primary structures in the brain are expressed highest in the embryonic mouse. Proteins involved in the development of the brain are expressed highest in the juvenile phase and proteins that make utilization of the brain possible by delivering energy are expressed highest in the adult mice.

Aging↗
PubMed2005

Dimeric dUTPases, HisE, and MazG belong to a new superfamily of all-alpha NTP pyrophosphohydrolases with potential "house-cleaning" functions.

Structure-guided analysis of the new dimeric dUTPase family revealed its sequence relationship to the phage T4 dCTPase, phosphoribosyl-ATP pyrophosphatase HisE, NTP pyrophosphatase MazG, and several uncharacterized protein families, including the human protein XTP3TPA (RS21-C6), which is overexpressed in embryonic and cancer cells. Comparison with the recently determined structure of a MazG-like protein from Sulfolobus solfataricus supported the unification of these enzymes in one superfamily of all-alpha NTP pyrophosphatases, suggesting that dimeric dUTPases evolved from a tetrameric MazG-like ancestor by gene duplication. Analysis of the structure of the Sulfolobus MazG points to 2-hydroxyadenosine (isoguanosine) triphosphate, a product of oxidative damage of ATP, as the most likely substrate. We predict that uncharacterized members of this superfamily perform "house-cleaning" functions by hydrolyzing abnormal NTPs and are functionally analogous to the structurally unrelated hydrolases of the Nudix superfamily. We outline probable tertiary and quaternary structures of the all-alpha NTP pyrophosphatase superfamily members.

Amino Acid Sequence↗
PubMed1999

Binuclear Drosophila oocytes: consequences and implications for dorsal-ventral patterning in oogenesis and embryogenesis.

The position of the nucleus along the anterior rim of stage 8 Drosophila oocytes presages the dorsal side of the egg and the developing embryo. In this paper, we address the question of whether the oocyte has a previously determined dorsal side to which the nucleus is drawn, or whether nuclear position randomly determines the dorsal side. To do so, we have taken advantage of a genetic system in which Drosophila oocytes occasionally become binuclear. We find that (i) the two nuclei migrate independently to their respective positions on the anterior rim, sometimes selecting the same site, sometimes not, (ii) the two nuclei are equivalent in their ability to induce a dorsal-ventral pattern in the overlying follicular epithelium, and (iii) at any position around the anterior circumference of the egg chamber the follicle cell sheet is equally responsive to the Gurken signal associated with the oocyte nuclei. These results argue that the dorsal-ventral axis is determined arbitrarily by the randomly selected position of the nucleus on the anterior rim of the oocyte. Some of the binuclear eggs support embryonic development. However, despite the duplication of dorsal chorion structures, the majority of such embryos show normal dorsal-ventral patterning. Thus, processes exist in the ventral follicular epithelium or in the perivitelline space that compensate for the expansion of dorsal follicle cell fates and consequently allow the formation of a normal embryonic axis.

Animals↗
PubMed1988

The albino deletion complex and early postimplantation survival in the mouse.

The albino deletion complex in the mouse represents 37 overlapping chromosomal deficiencies that have been arranged into at least twelve complementation groups. Many of the deletions cover regions of chromosome 7 that contain genes necessary for early embryonic development. The work reported here concentrates on two of these deletions (c6H, c11DSD), both of which were known to be lethal around the time of gastrulation when homozygous. A detailed embryological analysis has revealed distinct differences in the lethal phenotype associated with the c6H and c11DSD deletions. c6H homozygous embryos are grossly abnormal at day 7.5 of gestation, whereas c11DSD homozygous embryos appear abnormal at day 8.5 of gestation. There is no development of the extraembryonic ectoderm in c6H homozygotes, whereas extensive development of this tissue type occurs in c11DSD homozygotes. The visceral endoderm is abnormally shaped and the parietal endoderm appears to be overproduced in c6H homozygotes; these structures are not affected in c11DSD homozygotes. The embryonic ectoderm is runted in both types of embryo and it is not possible to obtain homozygous embryo-derived stem-cell lines for either deletion. Mesoderm formation occurs in the c11DSD but not in the c6H homozygotes. The c11DSD deletion chromosome complements the c6H chromosome in that the lethal phenotype of the compound heterozygote is similar to that of the c11DSD homozygote. These results suggest that a gene(s) necessary for normal development of the extraembryonic ectoderm is present in the c11DSD but deficient in the c6H deletion chromosome.

Albinism↗
PubMed1987

Hexabrachion proteins in embryonic chicken tissues and human tumors.

Cell cultures of chicken embryo and human fibroblasts produce a large extracellular matrix molecule with a six-armed structure that we called a hexabrachion (Erickson, H. P., and J. L. Iglesias, 1984, Nature (Lond.), 311:267-269. In the present work we have determined that the myotendinous (M1) antigen described by M. Chiquet and D. M. Fambrough in chicken tissues (1984, J. Cell Biol., 98:1926-1936), and the glioma mesenchymal extracellular matrix protein described by Bourdon et al. in human tumors (Bourdon, M. A., C. J. Wikstrand, H. Furthmayr, T. J. Matthews, and D. D. Bigner, 1983, Cancer Res. 43:2796-2805) have the structure of hexabrachions. We also demonstrate that the M1 antigen is present in embryonic brain, where it was previously reported absent, and have purified hexabrachions from brain homogenates. The recently described cytotactin (Grumet, M., S. Hoffman, K. L. Crossin, and G. M. Edelman, 1985, Proc. Natl. Acad. Sci. USA, 82:8075-8079) now appears to be identical to the chicken hexabrachion protein. In a search for functional roles, we looked for a possible cell attachment activity. A strong, fibronectin-like attachment activity was present in (NH4)2SO4 precipitates of cell supernatant and sedimented with hexabrachions in glycerol gradients. Hexabrachions purified by antibody adsorption, however, had lost this activity, suggesting that it was due to a separate factor associated with hexabrachions in the gradient fractions. The combined information in the several, previously unrelated studies suggests that hexabrachions may play a role in organizing localized regions of extracellular matrix. The protein is prominently expressed at specific times and locations during embryonic development, is retained in certain adult tissues, and is reexpressed in a variety of tumors.

Animals↗
PubMed1990

A mouse macrophage factor induces head structures and organizes a body axis in Xenopus.

Soluble peptide factors have been implicated as the agents responsible for embryonic inductions in vertebrates. Here, a protein (PIF) secreted by a mouse macrophage cell line is shown to change the developmental fate of Xenopus embryonic cells. Exposure to PIF causes presumptive ectodermal explants to form anterior neural and mesodermal tissues, including brain and eye, instead of ciliated epidermis. In addition, the induced tissues are organized into a rudimentary embryonic axis. These results suggest that PIF or a closely related molecule is involved in inducing anterior structures and organizing the frog body plan.

Animals↗
PubMed2003

p19Arf-p53 tumor suppressor pathway regulates cell motility by suppression of phosphoinositide 3-kinase and Rac1 GTPase activities.

The p19(Arf)-p53 tumor suppressor pathway plays a critical role in cell-cycle checkpoint control and apoptosis, whereas Rho family small GTPases are key regulators of actin structure and cell motility. By using primary mouse embryonic fibroblasts that lack Arf, p53, or both, we studied the involvement of the p19(Arf)-p53 pathway in the regulation of cell motility and its relationship with Rho GTPases. Deletion of Arf and/or p53 led to actin cytoskeleton reorganization and a significant increase in cell motility. The endogenous phosphoinositide (PI) 3- kinase and Rac1 activities were elevated in Arf(-/-) and p53(-/-) cells, and these activities are required for p19(Arf)- and p53-regulated migration. Reintroduction of the wild type Arf or p53 genes into Arf(-/-) or p53(-/-) cells reversed the PI 3-kinase and Rho GTPase activities as well as the migration phenotype. These results suggest a functional relationship between an established tumor suppressor pathway and a signaling module that controls actin structure and cell motility and show that p19(Arf) and p53 negatively regulate cell migration by suppression of PI 3-kinase and Rac1 activities.

Animals↗
PubMed1995

Complex asparagine-linked oligosaccharides in Mgat1-null embryos.

To investigate the developmental role of complex N-linked oligosaccharides, we previously inactivated the mouse Mgat1 gene which encodes UDP-N-acetylglucosamine: alpha-3-D-mannoside beta-1,2-N-acetylglucosaminyltransferase I (GlcNAc-TI). Mgat1-null embryos developed morphogenic abnormalities by embryonic day (E) 9.5 and failed to survive beyond E10.5. Prior to E8.5, mutant and wild-type embryos were phenotypically indistinguishable, raising the unexpected possibility that earlier embryonic development may not require complex N-glycans. We have now used in situ RNA hybridization to assess the temporal and spatial pattern of Mgat1 expression in normal embryos, and lectin histochemistry to determine whether Mgat1-null embryos lack complex N-glycans at pre-E9.5 developmental stages. In situ RNA analysis indicated that Mgat1 transcripts normally increase dramatically between E7.0 and E9.5, 1-2 days prior to the death of mutant embryos. However, apparently normal levels of complex N-glycans were observed in E3.5 pre-implantation Mgat1-null embryos prior to declining to undetectable levels by E7.5. Complex N-glycans were not observed in E7.5-E9.5 Mgat1-null embryos with the notable exception of vesicular structures within cells of the visceral extra-embryonic endoderm, perhaps reflecting the ability of these cells to take up and transport maternally derived glycoproteins. Mgat1-null embryos appear to complete pre-implantation development in the presence of maternally derived complex N-glycans, and may die at later stages, post E7.5, when a requirement for embryonically derived complex N-glycans arises.

Animals↗
PubMed2000

Paternal exposure to cyclophosphamide alters cell-cell contacts and activation of embryonic transcription in the preimplantation rat embryo.

Paternal exposure to chronic low doses of cyclophosphamide, an anticancer agent, results in aberrant embryonic development of the progeny. We hypothesized that paternal exposure to cyclophosphamide disturbs zygotic gene activity regulating proper progression through preimplantation development and that this disturbance results in improper cell-cell interactions. To test this hypothesis, we analyzed cell-cell interactions and the expression of cytoskeletal elements in preimplantation embryos sired by male rats gavaged with saline or 6 mg kg(-1) day(-1) cyclophosphamide for 5 wk. Embryos from control litters had 4-12 cells on Day 2 of gestation; cell-cell contacts were observed consistently. Embryos from litters sired by cyclophosphamide-treated males were frequently abnormal and had lower cell numbers and decreased cell-cell contacts. Steady state concentrations of the mRNAs for cell adhesion molecules (cadherins and connexin 43) and structural proteins (beta-actin, collagen, and vimentin) were low in two- and four-cell control embryos; expression increased dramatically by the eight-cell stage. In contrast, embryos sired by cyclophosphamide-treated males displayed the highest expression of most trancripts at the two-cell stage. In parallel with the mRNA profiles, E-cadherin immmunoreactivity was nearly absent in two-cell control embryos and was strong by the eight-cell stage; immunoreactivity in embryos sired by drug-treated fathers was strong at the two-cell stage but absent at later stages. Thus, drug exposure of the paternal genome led to dysregulated expression of structural elements and decreased cell interactions during preimplantation embryonic development.

Animals↗
PubMed2000

The mouse zona pellucida: folliculogenesis, fertility and pre-implantation development.

Perinatally, oocytes within the mouse ovary become surrounded by a layer of flattened granulosa cells and form primordial follicles. The subsequent accretion of the zona pellucida between the oocytes and granulosa cells provides a biochemical marker of folliculogenesis. In mice, the zona matrix is composed of three proteins (ZP1, ZP2, ZP3). Mouse lines lacking either ZP1 or ZP3 have been established and have abnormal folliculogenesis. Without ZP1, structurally defective zonae are formed resulting in decreased fecundity due to early embryonic loss. More strikingly, without ZP3, the zona matrix is absent, no 2-cell embryos are formed and females are infertile. The structural integrity of the zona matrix can be restored by substituting human homologues for the missing mouse protein and these 'humanized' zona matrices should prove useful in investigating the molecular basis of fertilization.

Animals↗
PubMed2005

Differential expression of the duplicated cellular retinoic acid-binding protein 2 genes (crabp2a and crabp2b) during zebrafish embryonic development.

The cellular retinoic acid-binding protein 2 (CRABP2) is believed to be involved in regulating access of retinoic acid to nuclear retinoic acid receptors. We have determined the cDNA sequence and the genomic organization of the duplicated crabp2 gene (crabp2b) in zebrafish. The crabp2b cDNA was 522bp in length and encodes a polypeptide consisting of 146 amino acids. Radiation hybrid mapping assigned the crabp2b gene to zebrafish linkage group 19. The comparison of the mapped human CRABP2 gene, zebrafish crabp2a and zebrafish crabp2b genes revealed that human chromosome 1 has a syntenic relationship to zebrafish linkage groups 16 and 19. Reverse transcription-polymerase chain reaction (RT-PCR) detected crabp2b mRNA in total RNA extracted from whole adult zebrafish, but not in any of the adult zebrafish tissues examined. The crabp2a mRNA was detected in total RNA extracted from whole adult zebrafish, adult zebrafish muscle, testes, and skin and to a lesser extent in heart, ovary and brain. No crabp2a mRNA-specific product was detected in kidney, liver or intestine of the adult zebrafish. Whole mount in situ hybridization detected crabp2b and crabp2a mRNA in a number of structures known to require retinoic acid signaling during embryonic development. The crabp2b mRNA was detected in the central nervous system, branchial arches, pectoral fins, retina (dorsal to the lens), epidermis and otic vesicle of the developing zebrafish. The crabp2a transcripts were detected by whole mount in situ hybridization in the central nervous system, epidermis, proliferative zone of the retina, intestinal bulb, oesophagus, pectoral fins and branchial arches during zebrafish embryonic development.

Amino Acid Sequence↗
PubMed2001

Retinoid X receptor alpha and retinoic acid receptor gamma mediate expression of genes encoding tight-junction proteins and barrier function in F9 cells during visceral endodermal differentiation.

Retinoids are critical for differentiation of columnar epithelial cells and for preventing metaplasia of these cells into stratified squamous epithelial cells, in which tight junctions (TJs) are essentially absent. This implies that retinoids might play important roles in regulating the structures and functions of TJs of columnar epithelium. F9 murine embryonal carcinoma cells differentiate into epithelial cells resembling visceral endoderm bearing TJs, when grown in suspension as aggregates in the presence of retinoic acid (RA). We show that RA induces the TJ structure and expression of several TJ-associated molecules, such as ZO-1, occludin, claudin-6, and claudin-7, as well as a barrier function in the genetically engineered cell line F9:rtTA:Cre-ER(T) L32T2, which allows sophisticated genetic manipulations simply by addition of ligands (H. Chiba et al., 2000, Exp. Cell Res. 260, 334-339). Interestingly, our data indicate that a barrier for small substances is generated after that for large ones during de novo formation of TJs. We also compared the RA-induced expression of TJ components and barrier function in RXRalpha(-/-)-RARgamma(-/-) F9 cells with those in wild-type cells and show that the retinoid signals for transduction of these events are mediated by specific RXR-RAR pairs.

Animals↗
PubMed1988

The Claude Bernard lecture, 1987. Embryonic chimeras: a tool for studying the development of the nervous and immune systems.

Chimeras have been constructed in the avian embryo following the observation of the particular structure of the interphase nucleus in the Japanese quail (Coturnix coturnix japonica). In all embryonic and adult cell types of this species a large amount of heterochromatin is associated with the nucleolus, making quail cells readily distinguishable from those of the chick where the constitutive heterochromatin is evenly dispersed in the nucleus. These structural differences have been used to devise a cell-marking technique through which cell migrations and cell interactions during embryogenesis can be followed in the embryo in ovo by grafting quail cells into chick embryos or vice versa. This method was applied to the ontogeny of the neural crest and of the immune system. Recently quail-chick chimeras have been allowed to hatch and the immunological status of the embryonic grafts after birth scrutinized. Xenogeneic tissue grafts made in the embryo are rejected after birth with a more or less prolonged delay according to the nature of the graft. However, rejection can be prevented and a permanent state of tolerance induced for the embryonic tissue grafts by isotopically implanting the thymic epithelium from the same quail donor.

Animals↗
PubMedDate not supplied

Early development of the neural plate, neural crest and facial region of marsupials.

Marsupial mammals have a distinctive reproductive strategy. The young are born after an exceptionally short period of organogenesis and are consequently extremely altricial. Yet because they must be functionally independent in an essentially embryonic condition, the marsupial neonate exhibits a unique suite of adaptations. In particular, certain bones of the facial region, most cranial musculature and a few additional structures are accelerated in their development. In contrast, central nervous system structures, especially the forebrain, are markedly premature at birth, resembling an embryonic d 11 or 12 mouse. This review examines the developmental processes that are modified to produce these evolutionary changes. The focus is on the early development of the neural plate, neural crest and facial region in the marsupial, Monodelphis domestica, compared with patterns reported for rodents. Neural crest begins differentiation and migration at the neural plate stage, which results in large accumulations of neural crest in the facial region at an early stage of development. The early accumulation of neural crest provides the material for the accelerated development of oral and facial structures. The first arch region is massive in the early embryo, and the development of the olfactory placode and frontonasal region is advanced relative to the forebrain region. The development of the forebrain is delayed in marsupials relative to the hindbrain or facial region. These observations illustrate how development may be modified to produce evolutionary changes that distinguish taxa. Further, they suggest that development is not necessarily highly conserved, but instead may be quite plastic.

Adaptation, Physiological↗
PubMed1988

Prenatal toxicity of acyclovir in rats.

Pregnant rats were treated during organogenesis with s.c. injections of acyclovir and the embryos were evaluated on day 11.5 of gestation (crown-rump length, somites, protein content, score, abnormalities, histological examination). After eight injections of 50 mg/kg body wt on days 9, 10, and 11 of pregnancy a reduction of the crown-rump length was noticed. After 100 mg/kg this effect was more pronounced. With two or three applications of this dose on day 10 specific embryonic abnormalities were visible: the shape of the head was abnormal, the width of the skull had decreased resembling a beak-like visceral cranium. With a single administration of 200 mg/kg on day 10 we found a similar but slightly more pronounced outcome. A drastic change of all variables was obtained after eight injections of 100 mg/kg on days 9, 10, and 11. Comparatively we measured maternal plasma concentrations of acyclovir 1 h after the administration of 50, 100 or 200 mg/kg body wt. After an injection of 50 mg/kg on days 9, 10, and 11 of gestation (three injections/day) the plasma levels ranged from 19.1 to 40.0 mg/l (1 mg/l = 4.44 microM). No cumulation was observed. In contrast, a cumulative effect was detected following a dose of 100 mg/kg. After the first injection of this dose a mean value (+/- SD) of 60.3 +/- 14.7 mg/l (n = 16) was obtained. In this case a third injection increased the mean plasma level to 124.6 +/- 16.6 mg/l (n = 5). Further injections, however, led to decreasing levels. One hour after administration of 200 mg/kg body wt acyclovir levels ranged from 120.0 to 163.9 mg/l. We conclude that acyclovir, at doses leading to plasma concentrations well above the therapeutic level in the dam, interferes with the embryonic development in the rat. Acyclovir induces typical gross structural abnormalities which have been first observed using a whole embryo culture system.

Acyclovir↗
PubMed1997

The survival of embryonic cardiomyocytes transplanted into damaged host rat myocardium.

In this study, attempts were made to replace damaged myocardium of adult rats with embryonic grafts. To this purpose pieces of embryonic ventricular myocardium were prelabelled with 4',6-diamidino-2-phenylindole and placed into a damaged area of the host myocardium. The hearts containing the grafts were then examined between 2 days and 5-7 months later. Initially the 4'-6-diamindino-2-phenylindole labelled cells were localized only at the site of grafting, but by 2-5 weeks they migrated along the ventricular surface of the heart. Nevertheless the greatest density of grafted cells was always found in the damaged area. At all time points studied, the myogenic phenotype of the 4'-6-diamindino-2-phenylindole-labelled cells was maintained, as the cells contained myosin heavy chains. In addition, immunolabelling with antibodies against cardiac gap junction proteins revealed that initially gap junctions were scattered within the transplanted tissue but with time they became more organised, firstly by alignment into rows along the developing myofibres and then into structures that resembled intercalated discs. Thus the grafted embryonic cardiac myocytes survived in an adult host myocardium and expressed characteristics typical of heart cells.

Animals↗
PubMed1996

Restricted expression of R-cadherin by brain nuclei and neural circuits of the developing chicken brain.

Cadherins are a family of Ca(2+)-dependent cell-cell adhesion molecules regulating morphogenesis by a preferentially homophilic binding mechanism. We have previously shown that the expression of R-cadherin in the early chicken forebrain (embryonic days E3-E6) is restricted to particular neuromeres or parts of neuromeres. R-cadherin-expressing neuroblasts born in these areas accumulate in the mantle zone and aggregate in particular (pro-) nuclei (Gänzler and Redies [1995] J. Neurosci. 15:4157-4172). In the present study, these findings are extended to later developmental stages (embryonic days E8, E11, and E15). By immunohistochemical and in situ hybridization techniques, we show that, at these stages of development, R-cadherin expression remains restricted to particular developing gray matter regions and fiber tracts. The R-cadherin-positive fiber tracts connect some of the R-cadherin-positive gray matter areas to form parts of particular neural circuits in the visual, auditory, somatosensory, and motor systems. Moreover, R-cadherin expression reflects the morphologic differentiation of gray matter regions. As brain nuclei become morphologically more distinct, the expression of R-cadherin shows a clearer demarcation of the nuclear boundaries. In addition, R-cadherin expression in some nuclei becomes restricted to particular subregions or to clusters of neurons. In the cerebellum, R-cadherin is expressed in parasagittal stripes. These results suggest that R-cadherin expression reflects the functional and morphologic maturation of gray matter structures and of information processing circuits in the embryonic chicken brain.

Animals↗