bluuebunny/crossref_metadata_2025_split huggingface dataset:
Segregation and early dispersal of neural crest cells in the embryonic zebrafish
Authors: Raible David W. , Wood Andrew , Hodsdon Wendy , Henion Paul D. , Weston James A. , Eisen Judith S. 
Published: February 2005

AbstractWe have exploited our ability to visualize and follow individual cells in situ, in the living embryo, to study the development of trunk neural crest in the embryonic zebrafish. In most respects, the development of zebrafish trunk neural crest is similar to the development of trunk neural crest in other species: zebrafish trunk neural crest cells segregate from the dorsal neural keel in a rostrocaudal sequence, migrate ventrally along two pathways, and give rise to neurons of the peripheral nervous system, Schwann cells, and pigment cells. However, some aspects of the development of zebrafish trunk neural crest differ from those of other vertebrates: zebrafish trunk neural crest cells are significantly larger and fewer in number than those in avian embryos and the locations of their migratory pathways are slightly different. This initial description of neural crest development in the zebrafish embryo provides the foundation for future experimental studies. © 1992 Wiley‐Liss, Inc.
Cellular contribution of the different regions of the somatopleure to the developing limb
Authors: Geduspan Jene S. , Solursh Michael 
Published: February 2005

AbstractRegionalization of the presumptive limb region was examined before and at the onset of limb development by means of a variety of transplantation experiments between quail and chick embryos in ovo. The results demonstrate a two‐step process, the first of which is the designation of the region of the somatopleure that would become part of the limb, followed by specification of dorsal and ventral regions of the limb. The medial half of the somatic mesoderm is the region which gives rise to the limb with only a smaller cellular contribution from the lateral half of the somatic mesoderm. The cellular contribution of the medial region of the somatopleure appeared to determine the type of limb formed (i.e., wing or leg). The second process relates to changes in the ability of the somatic ectoderm to undergo extensive lateral displacement with development. Starting at stage 14, the medial and lateral somatic ectoderms maintain their position after transplantation, in contrast to earlier stage limb or flank ectoderms which undergo extensive lateral displacement with development. The positional determination of the dorsal and ventral properties of the medial and lateral ectoderms of the prospective limb region and their distal displacement during limb outgrowth may be important morphogenetic events in limb development. © 1993 Wiley‐Liss, Inc.
Cell interactions influence the pattern of biomineralization in the Ilyanassa obsoleta (mollusca) embryo
Authors: McCain Elizabeth R. 
Published: February 2005

AbstractIlyanassa obsoleta larvae have two calcium carbonate‐containing organs, shell and statocyst, which are derived from five micromere cells (2a, 2c, 2d, 3c, 3d). “Internal shell,” an abnormal, internal calcium carbonate mass, was previously observed when cells which normally induce shell and statocyst were removed. This study utilizes multiple‐cell deletions to examine how these calcium carbonate‐producing precursors control the pattern of biomineralization, whether it is in external shell, statocyst, or internal shell. It was demonstrated that internal shell was solely derived from any of these five cells. However, there was a quantitative difference in the frequency of internal shell production depending upon which cells, as well as how many, are deleted. In general, when external shell or statocyst production was diminished, as the result of removing several of the calcium carbonate‐producing cells, internal shell was deposited instead. The presence of internal shell can best be explained as the result of altered interactions between these five cells after one or more have been deleted. Electron diffraction and transmission electron microscopy show that internal shell differs from normal shell in both structure and crystal morphology and it can also be produced by statocyst precursors. Thus, both the deletion and electron microscopy data support the interpretation that the development of internal shell is controlled by shell‐ and statocyst‐producing cells when the cell communication between these cells is disrupted. © 1993 Wiley‐Liss, Inc.
Pattern of expression of transforming growth factor‐β4 mRNA and protein in the developing chicken embryo
Authors: Jakowlew Sonia B. , Ciment Gary , Tuan Rocky S. , Sporn Michael B. , Roberts Anita B. 
Published: February 2005

AbstractExpression of TGF‐β4 mRNA and protein was studied in the developing chicken embryo using specific cDNA probes and antibodies for chicken TGF‐β4. Expression of TGF‐β4 mRNA was detected by day 4 of incubation (Hamburger and Hamilton stage 22, E4) by RNA Northern blot analysis and increased with developmental age until day 12 of incubation (stage 38, E12) where it was detected in every embryonic tissue examined, with expression being highest in smooth muscle and lowest in the kidney. The steady‐state level of expression of TGF‐β4 mRNA remained relatively constant in most embryonic tissues through day 19 (stage 45, E19). In situ hybridization analysis detected TGF‐β4 mRNA as early as the “definitive primitive streak” stage (stage 4); during neurulation (stage 10), TGF‐β4 mRNA was detected in all three germ layers, including neuroectoderm. Following neurulation, TGF‐β4 mRNA was detected in the neural tube, notochord, ectoderm, endoderm, sclerotome, and myotome, but not dermotome at stage 16. By day 6 of incubation (stage 29, E6), TGF‐β4 mRNA was localized in several tissues including heart, lung, and gizzard. Immunohistochemical staining analysis also showed expression of TGF‐β4 protein in all three germ layers as early as stage 4 in various cell types in qualitatively similar locations as TGF‐β4 mRNA. These results suggest that TGF‐β4 may play an important role in the development of many tissues in the chicken. © 1993 Wiley Liss, Inc.
Type II collagen during cartilage and corneal development: Immunohistochemical analysis with an anti‐telopeptide antibody
Authors: Chen Qian , Fitch John M. , Gibney Eileen , Linsenmayer Thomas F. 
Published: February 2005

AbstractWe have examined the pattern of immunoreactivity of a monoclonal antibody, II‐5B2, with specificity for an epitope which resides within the NH2‐terminal extension peptide (telopeptide) of the avian type II collagen molecule. This epitope is available in regions of matrix where de novo synthesis of the molecule is ongoing, but not where synthesis has ceased and maturation and crosslink formation have occurred. Within the cartilaginous growth plate, the epitope disappears from the matrix soon after the chondrocytes become hypertrophic; within the cornea, the epitope disappears subjacent to the epithelium. The II‐5B2 epitope is not made available by a variety of procedures shown to remove potentially masking substances and to disrupt fibrillar organization. It is rendered available, however, when covalent crosslink formation between collagen molecules is blocked through administration of β‐aminopropionitrile or penicillamine. In contrast, the epitope of another monoclonal antibody against type II collagen, II‐II6B3, which resides in the triple‐helical domain of the molecule, in cartilage is present throughout the growth plate including the hypertrophic zone, and in cornea extends for a considerable distance into the stroma. Thus, it is available for antibody binding regardless of fibril maturation and crosslinking. These data suggest that the II‐5B2 epitope becomes unavailable when the telopeptide becomes cross‐linked. By using these two monoclonal antibodies in serial sections, one can establish the crosslinking pattern of type II collagen in the tissue. This set of antibodies is a potentially useful tool for analyzing normal and abnormal development, remodeling, and repair processes in the skeletal system and in other tissues where type II collagen is involved in organization of the matrix, such as the primary corneal stroma. © 1993 wiley‐Liss, Inc.
Evidence that the border of the neural plate may be positioned by the interaction between signals that induce ventral and dorsal mesoderm
Authors: Zhang Jing , Jacobson Antone G. 
Published: February 2005

AbstractIn the early Xenopus embryo, a quadrant of endodermal cells that have descended from the vegetal dorsal localization in the zygote produces signals that pass into the animal hemisphere and induce dorsal mesoderm from the marginal zone. From the remaining three quadrants of the bordering endoderm, signals pass into the animal hemisphere and induce ventral mesoderm in the marginal region. There is evidence that suggests that these same mesoderm‐inducing signals continue through the plane of the tissue of the animal hemisphere where they may at least begin the processes of neural and epidermal induction by changing the competence of the prospective ectodermal cells, and possibly influencing the early regional biasing of later expression of at least some gene products, such as Epi‐1 whose expression in the future epidermal domain seems specified before gastrulation. We hypothesized that the interaction of the ventral and dorsal signals within the plane of the tissue of the animal hemisphere may position the border of the neural plate. If this is so, then transplantation into the animal pole of cells that signal induction of ventral mesoderm should drive the neural plate boundary back toward the blastopore and shorten the anterior‐posterior axis. Removal of cells that induce ventral mesoderm should result in an axis that is longer than normal. Results of our experiments support these predictions. Also, by late pregastrula stage 9, increasing the ventral signals has no effect. Thus the evidence suggests that the position of the anterior neural plate boundary is established before gastrulation begins by the interaction of the signals that induce the ventral and dorsal mesoderm. © 1993 wiley‐Liss, Inc.
Developmental expression of four novel serine/threonine kinase receptors homologous to the activin/transforming growth factor‐β type II receptor family
Authors: He Wei Wu , Gustafson Michael L. , Hirobe Seichii , Donahoe Patricia K. 
Published: February 2005

AbstractSerine/threonine kinase transmembrane proteins are a new family of growth factor signal transducers that includes several isoforms of the activin type II receptor and the type II receptor for transforming growth factor‐β. In an effort to clone the receptor for Mullerian inhibiting substance, a member of the transforming growth factor‐β superfamily, oligonucleotide primers designed from conserved regions of these receptors' kinase domains were used for PCR amplification of fetal rat urogenital ridge cDNA. We isolated four novel receptors in this manner (desingnated R1–R4), each of which has structural features of the previously cloned kinases, including a small extracellular ligand‐binding domain, a single hydrophobic transmembrane domain, and an intracellular serine/threonine kinase domain. In addition, each has characteristic kinase subdomains and conserved serine/threonine kinase sequences found in this family. Northern analysis revealed mRNA expression of R1‐R4 in several tissues, including fetal urogenital ridge, testis, and ovary, as well as brain and lung. In situ hybridization further localized R1 to mesenchyme of the 14.5 to 15‐day fetal rat Mullerian duct and to oocytes of preantral and antral follicles, sites that are consistent with the predicted localization of Mullerian inhibiting substance receptor. In addition, R2 localized specifically to seminiferous tubules of the postnatal testis. These newest members of the activin and transforming growth factor‐β type II receptor family should help define the molecular mechanisms by which this ligand superfamily affects cell growth and differentiation via membrane phosphorylation. © 1993 wiley‐Liss, Inc.
Developmental regulation and cell type‐specific expression of the murine γF‐crystallin gene is mediated through a lens‐specific element containing the γF‐1 binding site
Authors: Goring Daphne R. , Bryce Dawn Marie , Tsui Lap‐Chee , Breitman Martin L. , Liu Qiurong 
Published: February 2005

AbstractThe mouse γF‐crystallin gene, one of six differentially regulated members of the γ‐crystallin gene family, is expressed exclusively in central nuclear fiber cells of the adult lens. The expression of this gene is controlled through regulatory elements contained in two upstream enhancers and the proximal promoter. Here we show that while the upstream enhancers and the proximal promoter could each direct gene expression in fiber cells formed at early stages of lens growth and development, cooperation between these elements is required to achieve expression in fiber cells formed at later stages. Evidence is provided that cooperative interaction between these elements modulates gene expression by increasing promoter strength. We also show that sequences within the proximal promoter region that bind lens cell nuclear factor γF‐1 are sufficient to elicit gene expression in central nuclear fiber cells of the adult lens. © 1993 wiley‐Liss, Inc.
Early encounters of the repetitive kind: A prelude to cell adhesion in conjugating Tetrahymena thermophila
Authors: Brown Frederick , Tirone Sunlian , Wolfe Jason 
Published: February 2005

AbstractThe relationship between direct cell contacts and subsequent cell‐cell adhesion was studied in the ciliated protozoan, Tetrahymena thermophila. During sexual reproduction, adhesion into pairs begins at approximately 1 hr after mixing starved complementary mating types. However, direct contacts between cells prior to pairing are known to be required for the development of adhesion‐readiness. We find here that the initial contact interactions are necessary but not sufficient to drive the cells to adhesion‐readness. Secondary interactions are needed.Two distinct experimental strategies were used. First, we examined the effects of a mutant that is unable to pair but which can stimulate two different wild‐type mating type cells to pair when mixed. We showed that stimulation by the mutant is only partial; in response to mutant cells, wild‐Type cells ceased forming food vacuoles but did not undergo tip transformation or concanavalin A (Con A)‐receptor tipping. Further, kinetic analysis shows that when mixed together, pair‐formation among partially stimulated wild‐type cells is slightly delayed, allowing time for these pre‐pairing processes to occur. This indicates that, beyond the initial contact interaction, mutant‐stimulated wild‐type cells require a subsequent interaction which cannot be fulfilled by the mutants. Secondly, we found that by blocking contact interactions between wild‐type mating types at various time intervals after they were mixed, additional increase in tip transformation and Con A receptor tipping was prevented. Further, both processes underwent a regression. This indicates that multiple contact interactions are required to drive the cells to adhesion readiness and to prevent developmental slip‐back. © 1993 wiley‐Liss, Inc.
Re‐evaluating the role of astrocytes in blood‐brain barrier induction
Authors: Holash J. A. , Noden D. M. , Stewart P. A. 
Published: February 2005

AbstractNeural tissue induces brain capillary endothelial cells to express a diverse array of characteristics that allow them to regulate the passage of solutes between the blood and the brain; these features are collectively referred to as the blood‐brain barrier (BBB). Because astrocytes are intimately associated with brain capillaries, they have been thought to be the cell type responsible for barrier induction. Widely accepted support of this hypothesis has been derived from experiments showing that astrocytes implanted into the anterior chamber of the rat eye, or onto the chorioallantoic membrane of the chicken embryo, remain unstained by circulating Evan's blue, while grafts of fibroblasts in these sites stain intensely.We have found several limitations associated with placing grafts in either site, leading us to believe that previously reported results are inconclusive. Astrocytes implanted into the anterior chamber form grafts that are poorly vascularized, whereas fibroblast grafts are richly vascularized by vessels which are often fenestrated. This likely accounts for apparent differences in vessel permeability reported by others. We have found that iridial vessels associated with astrocyte grafts do not change their ultrastructure to resemble brain capillaries.Grafting of cells to the chorioallantoic membrane elicits an extensive inflammatory response. Inflammation results in poor delivery of tracers to graft vasculature as well as altering vessel permeability. Treatment of hosts with steroidal anti‐inflammatory agents in doses compatible with survival of the host does not resolve the inflammatory response but does allow improved graft survival. Even after treatment with anti‐inflammatory agents, however, astrocyte graft vasculature fails to express high levels of a barrier marker, the GLUT‐1 isoform of the glucose transporter. Transplantation of avascular embryonic spinal cord, that induces robust vessel ingrowth and GLUT‐1 expression in intra‐embryonic vessels, was unable to elicit the ingrowth of more than a few vessels from the chorioallantoic membrane vasculature, and none of these expressed glucose transporter. We conclude that the anterior chamber and chorioallantoic membrane are not suitable sites for studying BBB induction, and that there is, at present, no conclusive evidence that mature astrocytes play a significant role in the initial expression of the BBB. © 1993 Wiley‐Liss, Inc.
Development of the vasculature of the anterior pituitary: Ontogeny of basic fibroblast growth factor
Authors: Schechter Joel E. , Pattison Amy , Pattison Tim 
Published: February 2005

AbstractThis study correlates the ontogeny of basic fibroblast growth factor (FGF) with the development of the vasculature of the anterior pituitary (AP) in two strains of rat, Sprague‐Dawley (SD) and Fischer 344 (F344). Immunolocalization of FGF was followed from the first appearance of Rathke's pouch (RP) in 12‐day (12d) fetuses, through each day of fetal development, and in 5, 20, and 50d postnatal female rats. In addition, the ontogeny of folliculo‐stellate cells (FSC) is described, since previous studies suggested that these unique cells might function as phagocytes in the regulation of FGF. In both rat strains, vascularization of the AP commenced in 16d fetuses. In 15–20d fetuses, dense foci of immunopositivity for extracellular FGF were apparent at sites of capillary penetration adjacent to partially disrupted, immature gonadotropes. Localization of FGF was first detected in immature gonadotropes in 18d fetuses and persisted in the cytosol of a subpopulation of gonadotropes thereafter. In 15d fetuses, FGF was localized within the cytosol intimately associated with the peripheral‐facing plasma membranes of all cells of the adenohypophysis, and persisted to variable degrees in later fetal stages. Localization of FGF within nuclei of AP parenchymal cells was evident only in 16–17d fetuses. Although the ontogeny of FGF and vascularization of the AP was very similar in both rat strains, the ontogeny of FSC differed markedly. In both strains, follicular lumens contained FGF during late fetal and early postnatal development. However, both electron microscopy and immunostaining for S‐100 marker protein revealed that the postero‐lateral edges of the AP of F344 rats often lacked FSC when compared to SD rats, a situation which could compromise regulation of FGF by FSC at the AP periphery in that strain, and thereby contribute to the neovascularization from systemic blood vessels known to occur in that strain during prolactinoma formation. © 1993 Wiley‐Liss, Inc.
In situ hybridization studies suggest a role for the basic region‐leucine zipper protein hXBP‐1 in exocrine gland and skeletal development during mouse embryogenesis
Authors: Clauss Isabelle M. , Gravallese Ellen M. , Darling Jama M. , Shapiro Fred , Glimcher Melvin J. , Glimcher Laurie H. 
Published: February 2005

AbstractThe spatial and temporal distribution of transcripts for the TRE/CRE‐binding basic region‐leucine zipper protein hXBP‐1 was determined by in situ hybridization. Analysis of embryos from day 10.5 to 18.5 pc revealed high level expression of hXBP‐1 RNA in two developing organ systems: (1) in bone and cartilage cells of the developing skeleton and toothbuds, and (2) in exocrine glands including the pancreas and the submandibular and salivary glands. High level expression was also found in whisker follicles and in selected cells in brown adipose tissue. In the developing skeleton, hXBP‐1 RNA was expressed starting on day 11.5 pc in osteoblasts of newly formed intramembranous bone. Thereafter, hXBP‐1 was expressed in both osteoblasts and preosteoblasts in bone formed directly by intramembranous formation as well as in bone formed during endochondral ossification. The most intese signal was observed in preosteoblasts and osteoblasts of newly forming bone. At day 11.5 pc low level hXBP‐1 expression was also observed in matrix secreting chondroblasts of bones which are formed initially of cartilage, at the stage where they consist entirely of cartilage, at the stage where they consist entirely of cartilage. Signal was also present in matrix producing chondroblasts of the mature zone of the growth region during endochondral ossification although at significantly lower level than in osteoblasts. hXBP‐1 is thus the first transcription factor described, to our knowledge, whose level of expression is modulated during the osteoblast developmental sequence in vivo. The pattern of expression of hXBP‐1 in the developing skeleton was found to be very similar to that of the genes encoding the tissue inhibitor of metalloproteinase and alkaline phosphatase throughout development. These observations suggest that hXBP‐1 may play a role in regulating the expression of tissue specific genes (TIMP, osteonectin, osteopontin, osteocalcin) expressed in osteoblasts. It is intriguing that the promoter regions of several such genes contain potential hXBP‐1 binding sites. © 1993 Wiley‐Liss, Inc.