bluuebunny/crossref_metadata_2025_split huggingface dataset:
Colocalization of thrombospondin and syndecan during murine development
Authors: Corless Christopher L. , Mendoza Arturo , Collins Tucker , Lawler Jack 
Published: February 2005

AbstractThrombospondin is an adhesive glycoprotein that is thought to play a role in tissue genesis and repair. We have used a monoclonal anti‐thrombospondin antibody, designated 5G11, to localize thrombospondin in paraformaldehyde fixed, paraffin‐embedded sections of developing mouse embryos. Thrombospondin expression is observed in uterine smooth muscle, endometrial glands, the decidua, and trophoblastic giant cells during the initial phase of post‐implantation development in the embryo. Cardiac myocytes and neuroepithelial cells show positive staining for thrombospondin at day 8.5 of gestation, and this expression continues throughout the development of the myocardium and central nervous system. Strong staining for thrombospondin is seen in developing bone and in the liver. Thrombospondin is also observed in developing smooth muscle and skeletal muscle, as well as in a variety of epithelia, including the epidermis, small intestinal epithelium, lens epithelium, renal tubular epithelium, and the epithelium of the developing tooth. Comparison of thrombospondin staining with that of two known cell surface receptors for thrombospondin, syndecan and the vitronectin receptor, reveals remarkable colocalization of thrombospondin and syndecan in all tissues, but almost no coexpression with the vitronectin receptor. Coexpression of thrombospondin and syndecan may play an important role in cell‐cell or cell‐matrix interactions during development. © 1992 Wiley‐Liss, Inc.
Expression patterns of engrailed‐like proteins in the chick embryo
Authors: Gardner Charles A. , Barald Kate F. 
Published: February 2005

AbstractThe protein products of both of the identified chick engrailed‐like (En) genes, chick En‐1 and chick En‐2, are localized in cells of the developing brain, mandibular arch, spinal cord, dermatome, and ventral limb bud ectoderm, as demonstrated by labeling with the polyclonal antiserum αEnhb‐1 developed by Davis et al. (Development 111:281–298, 1991). A subpopulation of cephalic neural crest cells is also En‐protein‐positive. The monoclonal antibody 4D9 recognizes the chick En‐2 gene product exclusively (Patel et al.: Cell 58:955–968, 1989; Davis et al., 1991) and colocalizes with chick En‐2 mRNA in the developing head region of the chick embryo as shown by in situ hybridization (Gardner et al.: J. Neurosci. Res. 21:426–437, 1988). In the present study we examine the pattern of αEnhb‐1 and 4D9 localization throughout the chick embryo from the first appearance of antibody (Ab)‐positive cells at stage 8 (Hamburger and Hamilton: J. Morphol. 88:49–92, 1951) through stage 28 (1–5.5 days). We compare the localization patterns of the two Abs to each other, as well as to the localization of the monoclonal Ab, HNK‐1, which recognizes many neural crest cells, using double‐and triple‐label fluorescence immunohistochemistry. Most En protein‐positive cells in the path of neural crest cell migration are not HNK‐1 positive. In detailed examination of αEnhb‐1 and 4D9 localization, we find previously undetected patterns of En protein localization in the prechordal plate, hindbrain, myotome, ventral body‐wall mesoderm, and extraembryonic membranes. Based upon these observations we propose: (1) that En expression in the mesoderm may be induced through interaction with En expressing cells in the neuroectoderm; (2) that En expression in the head mesenchyme is associated with somitomere 4; and (3) that En expression may be involved in epithelial‐mesenchymal cell transformations. © 1992 Wiley‐Liss, Inc.
Changes in dorsoventral but not rostrocaudal regionalization of the chick neural tube in the absence of cranial notochord, as revealed by expression of Engrailed‐2
Authors: Darnell Diana K. , Schoenwolf Gary C. , Ordahl Charles P. 
Published: February 2005

AbstractNotochord has been implicated in previous studies in both the dorsoventral and rostrocaudal patterning of the developing neural tube. This possibility has been further explored by analyzing the expression of Engrailed‐2 in chick embryos developing with cranial notochord defects. Control embryos containing intact notochords expressed Engrailed‐2 protein within the neural tube and in a subset of the neural crest and overlying surface ectoderm at the future mesencephalon and cranial metencephalon levels. Within the neural tube, expression was confined to cell nuclei in the roof plate and lateral walls; floor plate nuclei directly overlying the notochord typically failed to show expression. After surgical removal of Hensen's node, the source of notochord precursor cells, embryos were cultured through neurulation and assayed for expression of Engrailed‐2 protein. All embryos that partially or completely lacked cranial notochord expressed Engrailed‐2 in a pattern similar to that of control embryos containing intact notochords, except that when notochord and floor plate were absent, Engrailed‐2 was also expressed in the most ventral part of the neural tube. These results indicate that (1) Engrailed‐2 expression is suppressed in the most ventral neural tube owing to induction of the floor plate by the notochord, and (2) that the presence of an underlying notochord is not required for correct rostrocaudal expression, suggesting that multiple pathways act in the patterning of the rudiment of the central nervous system. © 1992 Wiley‐Liss, Inc.
Expression of cell adhesion molecules during initiation and cessation of neural crest cell migration
Authors: Akitaya Tatsuo , Bronner‐Fraser Marianne 
Published: February 2005

AbstractBecause of their distribution and known ability to promote neuronal adhesion, it has been proposed that N‐CAM and N‐cadherin are involved in the formation of the nervous system. Here, we examine the expression of these molecules during the initiation and cessation of trunk neural crest cell migration during the formation of the peripheral nervous system. Whereas other neural tube cells express N‐cadherin, the dorsal neural tube containing neural crest precursors has little or no N‐cadherin immunoreactivity. In contrast, N‐CAM is expressed in the dorsal neural tube and on early migrating neural crest cells, from which it gradually disappears during migration. Both N‐CAM and N‐cadherin are absent from neural crest cells at advanced stages of migration. As neural crest cells cease migration and condense to form dorsal root and sympathetic ganglia, N‐cadherin but not N‐CAM is observed on the forming ganglia, identified by neurofilament expression and the aggregation of HNK‐1 reactive cells. The results demonstrate that the absence of N‐cadherin correlates with the onset of neural crest migration and its reappearance correlates with cessation of migration and precedes ganglio‐genesis. © 1992 Wiley‐Liss, Inc.
Coincident loss of mitochondria and nuclei during lens fiber cell differentiation
Authors: Bassnett Steven , Beebe David C. 
Published: February 2005

AbstractDuring normal differentiation, lens fiber cells lose their nuclei, mitochondria, and other membrane‐bound organelles. In the present study, a slice preparation of the embryonic chicken lens was used with laser scanning confocal microscopy to study the spatial and temporal patterns of organelle breakdown during embryonic development. At all stages examined, mitochondria in lens epithelial cells were present in perinuclear clusters. In contrast, early in development, lens fiber cells contained extremely elongated mitochondria (>100 μm) that were distributed throughout the cytoplasm and oriented along the long axis of the cells. By the 8th day of embryonic development (E8), the mitochondria in the central fiber cells began to fragment. At the same time, the nuclei in these cells became smaller and more spherical. By E10, mitochondrial staining in the central fibers became punctate. Electron microscopy of this region revealed swollen mitochondria with disrupted cristae. By E12, cells in the central region of the lens lacked mitochondria and nuclei. The loss of nuclei and mitochondria from a given cell was coincident and abrupt (2–4 hr), occurring in a previously unsuspected domain situated about 300 μm from the anterior surface of the lens. A cytoskeletal component, actin, persisted in the central cells indicating that organelle degradation represents a selective process and not simply the global degradation of supramolecular structures. Throughout embryonic development, the organelle‐free region grew at approximately the same rate as the lens and, by the time of hatching, had expanded to match the diameter of the pupil. The present results suggest that the embryonic lens will be a useful model system with which to study mechanisms of organelle degradation. © 1992 Wiley‐Liss, Inc.
Expression of NCAM isoforms during skeletal myogenesis in the mouse embryo
Authors: Lyons Gary E. , Moore Robert , Yahara Osamu , Buckingham Margaret E. , Walsh Frank S. 
Published: February 2005

AbstractWe have examined the developmental patterns of neural cell adhesion molecule (NCAM) gene expression in embryonic mouse skeletal muscle cells by in situ hybridization. Moreover, by utilising exon‐specific cRNA probes, we have examined tissue specific splicing of the NCAM gene. We show that there is a distinct sequence of NCAM isoform expression during skeletal muscle development. Since NCAMs are also expressed in other cell types, particularly neurons, NCAM mRNAs have been colocalised with acetylcholine receptor α (AChRα) gene transcripts to identify muscle‐specific expression. NCAM is first detected in somites as they first form, prior to their differentiation into muscle and nonmuscle compartments. Myotomes, the first skeletal muscle masses to form in the embryo, express mRNAs for the transmembrane 180 and 140 kDa isoforms of NCAM. Both of these transcripts are also detected in the neural tube, and their spatial pattern of expression changes with development. Transcripts containing the muscle‐specific domain (MSD) of the NCAM gene are not detected prior to 11 days postcoitum (p.c.), at a time when rostral somites already contain well‐developed myotomes. As the level of MSD mRNAs increases at 12 days p.c., the 140 and 180 kDa transcript levels decrease in skeletal muscle masses. The level of all NCAM isoform transcripts declines between 13 and 15 days p.c. in muscle. However, the 180 and 140 kDa NCAM isoforms are expressed at a high level in neural tissue and in other locations in the developing embryo such as in smooth muscle, around vibrissae follicles, and in the perichondrial zone of digits. © 1992 Wiley‐Liss, Inc.
Cardiac expression of polysialylated NCAM in the chicken embryo: Correlation with the ventricular conduction system
Authors: Watanabe Michiko , Timm Maureen , Fallah‐Najmabadi Hessam 
Published: February 2005

AbstractThe neural cell adhesion molecule (NCAM) and its polysialic acid moeity (PSA) affect cellular interactions during the development of the nervous system and skeletal muscle. NCAM has also been identified in the embryonic heart of various species including humans. However, knowledge regarding the role of NCAM and its function‐modulating PSA in cardiogenesis is limited. The distribution of NCAM and its PSA in the ventricular myocardium of chicken embryos was determined by indirect immunofluorescence staining. The NCAM polypeptide was found throughout the cardiac myocardium. In contrast PSA was located in discrete regions in stage 20 to 44 embryos (during and after septation). Myocardium at the subendocardial regions of the atrioventricular canal and ventricular trabeculae were PSA positive by stage 20. At later stages, transverse sections of the postseptation heart just below the level of the atrioventricular interface revealed a PSA‐positive bundle of myocardium in the septum. This bundle was continuous with two branches at a more apicallevel which in turn were continuous with the PSA‐positive subendocardial myocardium lining the left and right ventricles. This pattern of PSA in the myocardium was similar to that of the ventricular conduction system configuration defined in the adult heart. Electron micrographs of the subendocardium of the ventricular septum revealed PSA positivity on myofibril‐containing cells with the ultrastructural location of Purkinje fibers. At later stages (35–44) a subset of cells within PSA‐positive regions was stained by an antibody against an isoform of the myosin heavy chain found in adult Purkinje fibers. These cells and surrounding tissue lacked PSA in the adult heart. Thus polysialylated NCAM may be modulating cell–cell interactions during the development of the ventricular conduction system. © 1992 Wiley‐Liss, Inc.
Notochord of chick embryos secretes short‐form type IX collagen prior to the onset of vertebral chondrogenesis
Authors: Hayashi Masando , Hayashi Kimiko , Iyama Ken‐Ichi , Trelstad Robert L. , Linsenmayer Thomas F. , Mayne Richard 
Published: February 2005

AbstractThe notochord of embryonic chicks produces type IX collagen, as well as type II collagen, prior to the onset of vertebral chondrogenesis. To address the question of whether the notochord secretes the “long‐form” type IX collagen found in cartilage or the “short‐form” type IX found in the cornea and vitreous humor, we examined immunoreactivity of the notochordal type IX collagen using two different monoclonal antibodies. The antibody 2C2 recognizes an epitope close to the carboxyl‐terminus of the HMW fragment, which is present in both the long‐ and short‐form type IX collagens, whereas another antibody 4D6 recognizes an epitope in the NC4 domain of the long‐form type IX collagen, which is absent in the short‐form type IX collagen. Therefore, the long‐form is recognized by its reaction with both 2C2 and 4D6, while the short‐form by its reaction with only 2C2 and no reaction with 4D6. Immunostaining of vertebral sections with 2C2 shows an identical distribution of staining with that for type II collagen, although the staining with 2C2 is less intense. The 2C2‐reactive type IX collagen is found within the notochord at stage 14 and in the notochordal sheath at stage 20. Deposition of this collagen in the perinotochordal matrix increases with time and reaches a level comparable with that for type II at stage 31. In contrast, the 4D6‐reactive type IX collagen is not found within the notochord nor in the notochordal sheath. The collagen becomes detectable, however, in the perinotochordal matrix at stages 27 to 28 and is markedly increased at stage 29, reaching the levels for the 2C2‐reactive type IX at stage 31. A highly sensitive immuno‐dot blot assay has confirmed that the notochord from chick embryos at stages 19 to 20 produces type IX collagen that reacts with 2C2 but does not react with 4D6. The present study indicates (1) that the short‐form type IX collagen is secreted from the notochord and also from the sclerotome cells, and (2) that the switching in the production from the short‐form type IX collagen to the long‐form type IX occurs during stage 27 and stage 31 when sclerotome cells differentiate into chondrocytes in the developing vertebral body. © 1992 Wiley‐Liss, Inc.
The changing architecture of the neonatal rat ovary during histogenesis
Authors: Rajah Roopa , Glaser Edmund M. , Hirshfield Anne N. 
Published: February 2005

AbstractThe purpose of this study was to describe the changing histological organization of the rat ovary during postpartum days one through three (p1‐p3). A PC‐based image‐combining microscope system was used to reconstruct the ovary in three dimensions. On p1, cylindrical pocket‐like structures radiated from the core of the ovary that were open toward the surface epithelium. The walls of the pockets contained connective tissue cells and capillaries (stroma). By p2, these pockets had completely closed; each pocket enclosed a small nest of oocytes and a few presumptive granulosa cells. By p3, the pocket‐like organization had disappeared. On p1, only one or two primordial follicle‐like structures were observed in the core and toward the periphery of the ovary; most oocytes were not enclosed in follicles. By p3, very few naked oocytes remained; primordial follicles predominated in all the regions of the ovary and some of the follicles had multiple layers of granulosa cells. There were changes in location, area, and volume of the rete tubules during these postnatal days. The extraovarian rete was visible on all 3 days but changed its orientation relative to the ovary. The connecting rete was found beneath the epithelial layer of the ovary on all 3 days and showed dramatic increase in area on p2. The wide lumen of the intraovarian rete was in direct contact with some of the oocytes near by on all 3 days, but these “communication points” were most abundant on p2. Based on our observations of different cell–cell associations during this time period, we hypothesize (1) that the mesenchymal–presumptive granulosa cell association is essential for the completion of folliculogenesis, and (2) the rete ovarii may have an inductive role in follicle assembly. These observations suggest that the first 3 days postpartum are critically important for studying the heterogeneous cell interactions that lead to the assembly of primordial follicles. The regional differences in tissue organization during this formative period may have significant implications on later aspects of follicular development. © 1992 Wiley‐Liss, Inc.
Insertional mutation of a gene involved in growth regulation of the early mouse embryo
Authors: Iannaccone P. M. , Zhou X. , Khokha M. , Boucher D. , Kuehn M. R. 
Published: February 2005

AbstractA transgenic mouse strain derived from embryonic stem (ES) cells infected with multiple copies of a retroviral vector carries a recessive insertional mutation resulting in prenatal lethality. A detailed histological analysis of developing embryos has shown that the mutation results in hyperplasia of both embryonic and extraembryonic ectoderm and failure of mesoderm formation in the egg cylinder stage embryo. The number of cells in each lineage of normal and mutant embryos was estimated using stereological analysis of serial sections taken from implantation sites. We observed a 2‐fold increase in the number of embryonic ectoderm cells in mutant embryos at 7.5 days postcoitum (dpc). In addition, we found that mutant embryonic ectoderm cells are only 0.6 times as large as normal cells. The number of extraembryonic ectoderm cells in mutant embryos at 7.5 dpc is also increased, by almost 4‐fold. Mutant extraembryonic ectoderm cells are also smaller than normal, being only two‐thirds the size of wild‐type cells. The mutant phenotype suggests that the gene identified by this insertional mutation plays an important role in the growth control of early embryonic lineages. © 1992 Wiley‐Liss, Inc.
Development of olfactory nerve glia defined by a monoclonal antibody specific for schwann cells
Authors: Norgren Robert B. , Ratner Nancy , Brackenbury Robert 
Published: February 2005

AbstractAlthough there is considerable interest in the possible role of olfactory glia in the pathfinding abilities of olfactory nerve axons, the complete development of these glia in vivo has not been described. Using a specific Schwann cell marker, the 1E8 antibody, we have found that olfactory nerve glia can be identified throughout development. These glia appear to originate in the olfactory placode and migrate initially into the periphery of the olfactory nerve, and later into the center of the nerve. Olfactory nerve glia enter the presumptive olfactory bulb with the olfactory receptor neuron axons and distribute themselves along the edge of the olfactory nerve layer. The fact that olfactory nerve glia are specifically immunostained by the 1E8 monoclonal antibody, which recognizes the Schwann cell‐specific protein P0, suggests that these cells more closely resemble Schwann cells than astrocytes or enteric glia. These results support and extend previous findings suggesting that olfactory nerve glia have distinctive developmental and anatomical features which may be important to the regenerative capacity of the olfactory system. © 1992 Wiley‐Liss, Inc.
Puzzle of crystallin diversity in eye lenses
Authors: Piatigorsky Joram 
Published: February 2005

AbstractCrystallins have evolved by various mechanisms that are associated with high expression of their genes in the eye lens. The diversity and pattern of crystallins among different species indicate that independent events have occurred at the molecular level during the evolution of the lens in different invertebrates (jellyfish, squid, and octopus) and vertebrates. Although it is possible that different crystallins are needed to fulfill the specific needs of individual species, the unexpectedly large array of proteins that function as crystallins and their abundance in the lens raise the possibility that selective pressures optimizing the function of certain transcription factors in the lens contribute to the recruitment of crystallins. © 1993 wiley‐Liss, Inc.
Molecular control of glutamine synthetase expression in the developing retina tissue
Authors: Vardimon Lily , Ben‐dror Iris , Havazelet Nadav , Fox Lyle E. 
Published: February 2005

AbstractGlutamine synthetase is a differentiation marker of the neural retina, whose expression is restricted to Müller glia cells, is inducible by glucocorticoids and is dependent on tissue development. The retina tissue acquires the competence to express GS in response to glucocorticoids with development, although the level of hormone binding activity in the cells does not alter with age. Using CAT constructs that are controlled by “simple GRE” promoters we demonstrated that glucocorticoid receptor transcription activity in retina cells increases with development. The increase in receptor activity correlates directly with the increase in inducibility of the glutamine synthetase gene and inversely with the rate of retina cell proliferation. At early developmental ages, when retina cells are still proliferating, the glucocorticoid receptor is transcriptionally inactive and glutamine synthetase expression cannot be induced. Receptor activity increases progressively with development and by day 12, when cell proliferation ceases, competence for glutamine synthetase induction is high. This competence for glutamine synthetase induction can be repressed by overexpressing the oncogene v‐src, which stimulates retina cell proliferation. We discuss possible mechanisms for developmental‐dependent modulation of glucocorticoid receptor transcriptional activity. © 1993 wiley‐Liss, Inc.