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PubMed1995

Analysis of the neurofibromatosis 2 gene in human breast and hepatocellular carcinomas.

The neurofibromatosis 2 gene (NF2) mapped to chromosome 22q is a recently isolated tumor suppressor gene that participates in the tumorigenesis of cells of embryonic neural crest origin. The structural similarities between the NF2 product, merlin-schwannomin, and the band 4.1 family raise the possibility that merlin may participate in a wide range of cell activities, in which the cytoskeleton latticework has important roles to play. In order to examine the significance of NF2 in general carcinogenesis, comprehensive analyses of 68 cases of breast carcinoma, which shows frequent loss of heterozygosity at chromosome 22, and 48 hepatocellular carcinomas of different histological grade were performed. No mutation was detected by the polymerase chain reaction-single-strand conformation polymorphism method for six exons of NF2 in any of the cases examined, suggesting that NF2 may be less important in the tumorigenesis of breast and liver cancers than in that of cancers originating from the neural crest.

Base Sequence↗
PubMedDate not supplied

[The ultrastructure of the cell center in the enterocytes of mouse embryos and newborn mice].

The centrosome structure was studied in differentiating small intestine enterocytes of mouse embryos (day 16 to 17 of gestation) and newborn mice. It is shown that fine structure of the centrosome in embryonic enterocytes differs from that found in cells of the adult mice. The centrosome of the crypt cells is more active: a greater number of cytoplasmic microtubules terminates there; mother centriole has two types of satellites; both centrioles are surrounded by fine fibrillar material. In 20% of crypt cells, replication of centrioles is observed. In the upper part of the villus of embryonic intestine, there still are two centrioles per cell, but they are located 3-7 um apart and devoid of any cytoplasmic microtubules attached to or directed toward them. In newborn mice, centrosomes of cells located at the bottom of the crypt are less active, as compared with centrosomes of embryonic cells. There are 1-3 satellites on mother centriole and few cytoplasmic microtubules closing to the centrosome. In 20% of cells from the bottom of the crypt centrioles are replicating. In the lateral part of the crypt, centrosome is inactive: centrioles are located 1-3 um apart and do not replicate. In the villus, centrioles undergo changes similar to those observed in the villus of adult mice. Centrioles loose portions of microtubule triplets. Near the top of the villus, only one centriole was found in two of 25 studied cells. In the enterocytes of the murine small intestine, centrioles are always located far from nuclei and close to the apical cell surface (1-3 um from the brush border). Centrioles never form a primary cilium and are not attached to the plasma membrane.

Animals↗
PubMed1997

The human ALL-1/MLL/HRX antigen is predominantly localized in the nucleus of resting and proliferating peripheral blood mononuclear cells.

The ALL-1 gene is an important regulator of embryonal and hematopoietic development, and structural variants of the human gene generated by chromosomal translocations and other genomic alterations presumably act as oncogenes in the pathogenesis of acute leukemias and other hematological malignancies. Antisera against two different epitopes of the human ALL-1 protein (anti-ALL1-N and anti-ALL1-C) were produced. Both sera revealed indistinguishable patterns of antigen localization in human peripheral blood mononuclear cells (PBMCs). In resting PBMCs, the antigen was distributed in a speckled pattern across the nuclei, with an increased density at the nuclear envelope and the nuclear indentation. In mitotically stimulated PBMCs, the antigen surrounded the condensing chromosomes but did not colocalize with chromatin or the nuclear scaffold. The antigen is considered a marker for a novel nuclear subcompartment, a perichromosomal area termed the "chromosomal envelope." In Western blot experiments, the anti-ALL1-N serum reacted with a polypeptide corresponding to the expected full-length 430-kDa ALL-1 protein. Recombinant proteins representing the AT-hook and zinc binding subdomains of the ALL-1 protein interacted in vitro with a degenerate mixture of double-stranded oligodeoxynucleotides. Thus, the ALL-1 protein probably is a DNA-binding protein with both a sequence-unspecific (AT-hook) and a sequence-specific (zinc binding subdomains) double-stranded DNA binding mode.

Animals↗
PubMed1997

Avian visual lateralization: a review.

Cerebral asymmetries represent an important principle of the organization of nervous systems. The asymmetries of the avian visual system, with their partly complementary domains in the left and the right hemisphere, offer an excellent window for the lateralized learning and cognitive processes. These behavioural experiments are accompanied by biochemical, synaptic, electrophysiological and neuroanatomical studies which have clarified to some extent the neuronal foundations of this asymmetry. Additionally they show that most, but not all, aspects of visual lateralization depend on a minute asymmetry of prehatch visual stimulation which triggers a cascade of events transforming the embryonic nervous system into lateralized structure and functioning.

Animals↗
PubMed1997

A 3' remote control region is a candidate to modulate Hoxb-8 expression boundaries.

Hox genes have been shown to play a key role in the acquisition of positional identity by precursors of embryonic axial, paraxial and limb structures. This function is thought to depend on the sequential, concerted expression of these genes in time and space. However the underlying molecular mechanisms of this collinear expression are still largely unknown. So far we had identified proximal regulatory elements driving expression of Hoxb-8/LacZ transgenes in Hox-like expression patterns with rostral boundaries more posterior than those of the endogenous gene. In this work we have analyzed 30 kb of 3' genomic sequences for Hoxb-8 regulatory activity in transgenic mice. We have identified a control region in the Hoxb-5/b-4 intergenic region that rostrally extends the Hoxb-8/LacZ expression domain into the posterior hindbrain. In combination with the Hoxb-8 minimal promoter, the 3' control region drives transgene expression with boundaries more anterior than those of Hoxb-8 in the neural tube. When combined with a 4.5 kb Hoxb-8 upstream sequence, where essential proximal regulatory sequences are located, the 3' control region drives transgene expression in a domain which seems to correspond to that of the endogenous Hoxb-8. By deletion analysis we have narrowed down to 550bp the regulatory activity interacting with the Hoxb-8 minimal promoter. We discuss the possibility that this remote 3' enhancer, which is the closest regulatory region found in the cluster to rostrally extend Hoxb-8/LacZ expression, could be involved in the regulation of Hoxb-8 and interact with the proximal control elements.

Animals↗
PubMed1998

Structure and expression of a novel fibroblast growth factor, FGF-17, preferentially expressed in the embryonic brain.

We isolated the cDNA encoding a novel member (216 amino acids) of the fibroblast growth factor (FGF) family from rat embryos. As this protein is the 17th documented member of the FGF family, we tentatively termed it FGF-17. We have also determined the structures of mouse and human FGF-17 with high amino acid identity (100 and 98.6%) to rat FGF-17, respectively. Among FGF family members, FGF-17 is most similar (53.7% amino acid identity) to FGF-8. FGF-17 has a typical signal sequence at its amino terminus. As expected, recombinant rat FGF-17 was efficiently secreted by High Five insect cells infected with recombinant baculovirus containing the cDNA indicating that FGF-17 is a secreted protein. FGF-17 mRNA of approximately 2.1 kb was detected in rat embryos at E14.5, but not at E10.5 and E19.5 by Northern analysis. The mRNA was found to be preferentially expressed in the neuroepithelia of the isthmus and septum of the rat embryonic brain at E14.5 by in situ hybridization. The present results indicate that FGF-17 might be a novel secreted signaling molecule in the induction and patterning of the embryonic brain.

Amino Acid Sequence↗
PubMed2005

Lifetime changes in the vulva and vagina.

The morphology and physiology of the vulva and vagina change over a lifetime. The most salient changes are linked to puberty, the menstrual cycle, pregnancy, and menopause. The cutaneous epithelia of the mons pubis, labia, and clitoris originate from the embryonic ectoderm and exhibit a keratinized, stratified structure similar to the skin at other sites. The mucosa of the vulvar vestibule, which originates from the embryonic endoderm, is non-keratinized. The vagina, derived from the embryonic mesoderm, is responsive to estrogen cycling. At birth, the vulva and vagina exhibit the effects of residual maternal estrogens. During puberty, the vulva and vagina acquire mature characteristics in a sequential fashion in response to adrenal and gonadal maturation. A trend to earlier pubertal onset has been observed in Western developed countries. In women of reproductive age, the vaginal mucosa responds to steroid hormone cycling, exhibiting maximal thickness and intracellular glycogen content at mid-cycle. Vulvar skin thickness remains unchanged but menstrual cycle-associated changes in ortho- and parakeratosis occur at the cytological level. The vulva and vagina further adapt to the needs of pregnancy and delivery. After menopause, tissue atrophy ensues. Post-menopausal changes in skin barrier function, skin hydration, and irritant susceptibility have been observed on exposed skin but not on the vulva. Nevertheless, older women with incontinence are at increased risk for developing incontinence dermatitis. A combination of factors, such as tissue atrophy, slower dissipation of excess skin hydration, shear forces associated with limited mobility, and lower tissue regeneration capacity increase the risk of morbidity from incontinence dermatitis in older women.

Aging↗
PubMed2006

Functional analysis of CBP/p300 in embryonic orofacial mesenchymal cells.

CREB binding protein (CBP) and the close structural homolog, p300, are nuclear coactivators of multiple signaling pathways that play important roles in embryonic development and cellular homeostasis. TGFbeta regulates the proliferation rate of many cell types and has been demonstrated to inhibit the growth rate of mouse embryonic maxillary mesenchymal (MEMM) cells. The role of CBP and p300 in TGFbeta-mediated control of proliferation of MEMM cells was thus investigated using an in vitro gene knockdown approach. TGFbeta reporter assays demonstrated that p300 mRNA knockdown via targeted siRNAs led to a reduction in the response to TGFbeta, whereas knockdown of CBP by the same approach had an insignificant effect. In MEMM cell proliferation assays, siRNA-mediated knockdown of CBP and/or p300 had little impact upon TGFbeta-mediated growth inhibition; however, the basal rate of proliferation was increased. Inhibition of p300 activity via overexpression of a dominant-negative mutant (p300deltaC/H3) led to significant inhibition of TGFbeta-mediated activation of p3TP-lux. As with the siRNA knockdown approach, p300deltaC/H3 also increased the basal rate of cell proliferation of MEMM cells. CBP/p300 siRNA knockdown had a significant but incomplete inhibition of TGFbeta-induction of matrix metalloproteinase-9 (gelatinase B) expression. These data demonstrate that p300 is involved in Smad-mediated transcription of p3TP-lux, however, its role (and that of CBP) in biological processes such as the control of cell proliferation and extracellular matrix metabolism is more complex and may be mediated via mechanisms beyond coactivator recruitment.

Animals↗
PubMed1999

Structure-function analyses of thrombomodulin by gene-targeting in mice: the cytoplasmic domain is not required for normal fetal development.

Thrombomodulin (TM) is a widely expressed glycoprotein receptor that plays a physiologically important role in maintaining normal hemostatic balance postnatally. Inactivation of the TM gene in mice results in embryonic lethality without thrombosis, suggesting that structures of TM not recognized to be involved in coagulation might be critical for normal fetal development. Therefore, the in vivo role of the cytoplasmic domain of TM was studied by using homologous recombination in ES cells to create mice that lack this region of TM (TMcyt/cyt). Cross-breeding of F1 TMwt/cyt mice (1 wild-type and 1 mutant allele) resulted in more than 300 healthy offspring with a normal Mendelian inheritance pattern of 25.7% TMwt/wt, 46.6% TMwt/cyt, and 27.7% TMcyt/cyt mice, indicating that the tail of TM is not necessary for normal fetal development. Phenotypic analyses showed that the TMcyt/cyt mice responded identically to their wild-type littermates after procoagulant, proinflammatory, and skin wound challenges. Plasma levels of plasminogen, plasminogen activator inhibitor 1 (PAI-1), and alpha2-antiplasmin were unaltered, but plasmin:alpha2-antiplasmin (PAP) levels were significantly lower in TMcyt/cyt mice than in TMwt/wt mice (0.46 +/- 0.2 and 1.99 +/- 0.1 ng/mL, respectively; P <.001). Tissue levels of TM antigen were also unaffected. However, functional levels of plasma TM in the TMcyt/cyt mice, as measured by thrombin-dependent activation of protein C, were significantly increased (P <.001). This supported the hypothesis that suppression in PAP levels may be due to augmented activation of thrombin-activatable fibrinolysis inhibitor (TAFI), with resultant inhibition of plasmin generation. In conclusion, these studies exclude the cytoplasmic domain of TM from playing a role in the early embryonic lethality of TM-null mice and support its function in regulating plasmin generation in plasma.

Animals↗
PubMed1989

Differential expression of human HOX-2 genes along the anterior-posterior axis in embryonic central nervous system.

We have investigated the structure of the human HOX-2 locus, which encompasses a 90-kb region on chromosome 17q21. Five new human HOX-2 homeoboxes, termed HOX-2.5, 2.4, 2.6, 2.7 and 2.8, have been identified, and their nucleotide sequences are reported. They have the same 5'-3' transcriptional orientation and are clustered with three previously described HOX-2 homeoboxes (5'-2.5-2.4-2.3-2.2-2.1-2.6-2.7-2.8-3'). We have also investigated the region-specific expression of HOX-2 genes in human embryonic-fetal life by Northern-blot analysis. All genes are expressed in whole embryos and fetuses at 5-9 weeks from conception. Their major site of expression lies within the central nervous system (CNS), although they are transcribed at a lower level in body structures other than the CNS. Their relatively abundant expression in CNS has been analyzed along the anterior-posterior axis by dissecting the brain, the medulla oblongata and the spinal cord proper. HOX-2.5, 2.4 and 2.3 transcripts are markedly more abundant in spinal cord than in medulla, whereas 2.2, 2.1, 2.6 and 2.7 mRNAs are progressively more abundant in the medulla. Additionally, expression in brain was detected, although at lower level, for HOX-2.1, 2.6, 2.7, 2.8. Thus, the relative position of HOX-2 homeobox genes along the chromosome in the 5'-3' direction appears to correlate with the relative position of their expression domains along the CNS longitudinal axis in the caudal-cephalic direction.

Amino Acid Sequence↗
PubMed1992

Structural anomalies resulting from vascular disruption.

A diverse yet distinctive group of disorders and structural anomalies result from vascular disruption of embryonic and fetal blood vessels. The extent of damage, timing in gestation, and the mechanism of vascular disruption all determine the nature of the resultant structural anomalies. The developing human remains susceptible throughout pregnancy to teratogenic agents and events that alter uterine, placental, and embryonic or fetal circulation.

Abnormalities, Drug-Induced↗
PubMed2004

Embryonic and fetal programming of physiological disorders in adulthood.

In the past decade, data from numerous epidemiological studies have indicated strong inverse associations between birth weight and risk of coronary heart disease, hypertension, type 2-diabetes, and other diseases in adulthood. The "Barker hypothesis" thus postulates that a number of organ structures and functions undergo programming during embryonic and fetal life. This developmental programming determines the set points of physiological and metabolic responses in adult life. Alterations of nutrient availability during gestation may lead to developmental adaptations, via hormonal maneuvers by the embryo and fetus that readjust these set points. These adaptive measures have short-term benefits to the embryo and fetus, so that the newborn will be better prepared for the adverse environment (e.g., undernutrition). However, adequate nutritional support during postnatal life that enables catch-up growth may create metabolic conflicts that predispose the adult to aberrant physiological functions and, ultimately, increased risk of disease. It is plausible that other adverse in utero conditions, including exposure to developmental toxicants, may similarly alter adult disease susceptibility. This article provides an overview of the Barker hypothesis, its supporting evidence, the current advances in understanding the biological mechanisms underlying this phenomenon, and its implications for developmental toxicology.

Animals↗
PubMed1979

Sequences at the somatic recombination sites of immunoglobulin light-chain genes.

The entire nucleotide sequence of a 1.7-kilobase embryonic DNA fragment containing five joining (J) DNA segments for mouse immunoglobulin kappa chain gene has been determined. Each J DNA segment can encode amino acid residues 96--108. Comparison of one of the five J DNA sequences with those of an embryonic variable (V) gene and a complete kappa chain gene permitted localisation of a precise recombination site. The 5'-flanking regions of J DNA segments could form an inverted stem structure with the 3'-non-coding region of embryonic V genes. This hypothetical structure and gel-blotting analysis of total embryo and myeloma DNA suggest that the somatic recombination may be accompanied by excision of an entire DNA segment between a V gene and a J DNA segment. Antibody diversity may in part be generated by modulation of the precise recombination sites.

Animals↗
PubMed1975

[Development of the cloaca and its ulterior transformations in the polypterids (Pisces)].

Generally spoken cloacae have been but little studied. In Polypterus, a brachiopterygian fish, a cloaca only exists during parts of the embryonal and larval life and it gets replaced by structures consisting of an anus and an urinary sinus. In the beginning of embryonal life the posterior opening of the body seems to be nothing else than the original blastoporus. The wall of this opening acquires evaginations; the anlagen of the excretory ducts come in contact with them, establishing in that way a structure, that merits the name of cloaca. During the elongation of the post-vitellin body, the latter gets shifted from the level of metamere XII to that of metamere XXX. Another migration of the cloaca occurs when the digestive system acquires its development. Finally the cloaca may be found under the 47th and 48th muscular segments (at least in the species Polypterus senegalus senegalus Cuvier). During these stages the excretory ducts have build up an urinary sinus that gets separated from the gut. In adults no communication exists any more between the gut and the urinary sinus; the latter is a very destinct organ that may have an impair or pair aspect according to its being filled up. Because of the establishing of a communication with the genital ducts the sinus becomes an uro-genital sinus in the adult.

Animals↗
PubMed1989

Opposing microtubule- and actin-dependent forces in the development and maintenance of structural polarity in retinal photoreceptors.

We have used embryonic cells grown in vitro to study the roles of microtubules and microfilaments in the development and maintenance of the polarized shape of retinal photoreceptors. After several days in culture, isolated cone photoreceptors displayed a highly elongated, compartmentalized morphology similar to that of photoreceptors in vivo. When treated with the microtubule-depolymerizing agent nocodazole, these elongated photoreceptors became progressively shorter, eventually losing their compartmentalized structure and becoming round. Conversely, treatment with the actin-depolymerizing agent cytochalasin D caused the elongated photoreceptors to lengthen even further. Computer-assisted, quantitative analysis showed that responses of individual cells to both nocodazole and Cytochalasin D were concentration-dependent, graded, and reversible. Immunocytochemical studies suggested the presence of longitudinally oriented actin filaments and microtubules in these photoreceptors, prominent in the region that undergoes the most pronounced length changes in response to cytoskeletal inhibitors. Prior to becoming elongated, photoreceptor precursors could be accurately identified in early retinal cultures. These round cells undergo a stereotyped sequence of morphogenetic transformations during in vitro development, including elongation and compartmentalization of the cell body as well as extension of a single neurite. Treatment with either cytochalasin D or nocodazole completely blocked morphogenesis. In addition, cytochalasin D caused the development of an abnormal, elongated cell process, which formed by a microtubule-dependent mechanism. These nocodazole and cytochalasin D effects also were reversible. Taken together, these data indicate that the complex developmental transformations leading to photoreceptor polarization occur in the absence of intercellular contacts, and are predominantly controlled by intracellular cytoskeletal forces. They suggest the existence of continuously active, oppositely directed, microtubule- and actin-dependent forces, the balance of which is a determining factor in the development as well as the maintenance of the elongated, compartmentalized organization of photoreceptor cells.

Actins↗
PubMed1996

Cytogenetic and genetic studies of radiation-induced chromosome damage in mouse oocytes. I. Numerical and structural chromosome anomalies in metaphase II oocytes, pre- and post-implantation embryos.

The incidences of X-ray induced numerical and structural chromosome anomalies were screened in a range of developmental stages from metaphase II oocytes through to post-implantation embryos. Following 1 Gy of acute X-rays to immediately preovulatory stage oocytes, the rate of hyperploidy (chromosome gain) was found to be elevated over levels in unirradiated controls, at metaphase II, in 1-cell and 3.5 day pre-implantation embryos but not in 8.5 day post-implantation foetuses. In the latter, however, the frequency of mosiacism was significantly increased. A similar response of an increase in mosaicism but not in hyperploidy in 8.5 day post-implantation embryos was also found after irradiation of dictyate stage oocytes with 4 Gy of acute X-rays. Significantly elevated frequencies of structural chromosome anomalies were present in metaphase II oocytes and pre-implantation embryonic stages, but could not be detected in block-stained chromosome preparations from 8.5 day post-implantation foetuses. However, analysis of chromosome preparations after G-banding showed that almost 14% of 14.5 day foetuses carried a chromosome rearrangement after 1 Gy of X-rays to immediately preovulatory stage oocytes. Overall, our data indicate that the presence of radiation-induced chromosome gains are incompatible with embryonic survival but that a proportion of embryos with structural chromosome damage develop past mid-gestation. These latter embryos are therefore potentially capable of contributing to the genetic burden of the next generation.

Animals↗
PubMed1996

Chromatin and gene regulation at the onset of embryonic development.

Major transitions in chromosome and chromatin structure occur during development. Recent genetic and biochemical experiments demonstrate that these alterations in genome organization make significant contributions to establishing and maintaining states of differential transcriptional activity. Developmentally regulated changes in histone variants have a causal role in determining patterns of gene activity, directing the repression of specific eukaryotic genes. Chromosomal proteins such as Polycomb stabilize and maintain transcriptionally repressed states. Proteins regulating mitotic chromosome condensation have a role in determining the overall transcriptional activity of a chromosome. In this review, I place the developmental roles of these chromosomal constituents in a structural and functional context. Considerable insight now exists into the molecular mechanisms regulating chromosomal activity during development. Chromosomal architecture is emerging as a key controlling influence in the developmental regulation of gene expression. Recent genetic experiments using Caenorhabditis elegans, Drosophila melanogaster and the mouse have provided clear evidence for the functional differentiation of chromosomal structures during development. Chromosomes are visualized as highly specialized entities, within which the activity of particular domains is largely determined by defined structural proteins. At a more local level, the mechanisms regulating gene transcription during early embryogenesis in Xenopus and the mouse have been found to be dependent on the biochemical composition of individual nucleosomes. Thus, variation in the type and modification of chromosomal and chromatin structural proteins provides a dominant means of controlling the transcriptional activity of individual genes, individual chromosomal domains and of entire chromosomes. The focus of this review is to summarize these recent advances and to discuss their implications for developmental biology.

Animals↗
PubMed2002

Expression of the mouse gap junction gene Gjb3 is regulated by distinct mechanisms in embryonic stem cells and keratinocytes.

Connexins are the protein subunits of gap junction channels and are expressed in a highly regulated temporal and spatial pattern in embryonic development and adult life, with most cell types expressing more than one isoform. Connexin31 (Cx31) is encoded by the gene Gjb3 and expressed throughout mouse development n a complex pattern; in adult mice it becomes restricted to the granular layer of epidermis, testis, and placenta. In placenta, lack of Cx31 leads to transient dysmorphogenesis affecting embryonic survival. Here we have analyzed the structure of mouse Gjb3 as well as its transcriptional regulation by transient transfection of reporter gene constructs in HM1 mouse embryonic stem cells and a mouse keratinocytederived cell line, Hel37, as model systems for early development and skin, respectively. Like most connexin genes, Gjb3 is composed of two exons, the second of which contains the whole coding region and is separated from the first exon by an intron of 2.3 kb. Expression in keratinocytes is regulated by a basal promoter extending to 561 bp upstream of exon 1 in conjunction with a regulatory region between upstream positions 561 and 841. In contrast, expression of Gjb3 in embryonic stem cells depended on the basal promoter together with the intron. The enhancing effect of the intron was found only in embryonic stem cells and depended on its native position and the integrity of the splice sites. Thus, expression of Gjb3 in keratinocytes and embryonic stem cells is regulated by different cis-regulatory elements and differs in its requirements for the intron in situ.

Animals↗