bluuebunny/crossref_metadata_2025_split huggingface dataset:
Patterns of cell behaviour underlying somitogenesis and notochord formation in intact vertebrate embryos
Authors: Wood Andrew , Thorogood Peter 
Published: February 2005

AbstractWe have made a detailed analysis of cell behaviour using high resolution timelapse microscopy of the earliest cellular interactions taking place during morphogenesis of the notochord and somites in intact teleost embryos. Notochord formation is typified by active intercalation of paraxial mesenchyme cells into the lateral surfaces of the primordium. Following this recruitment phase, complete immiscibility develops between cells of the notochord and the presomitic mesenchyme. Dorso‐ventral and rostro‐caudal expansion of the notochord is characterised by translocation of cells within dorsoventral planes of section and is supported by elongation of the remaining cells and reduction in width across its latero‐medial axis. A lateral pallisading of paraxial mesenchyme against the lateral aspects of the notochord precedes overt segmentation. Intersomitic furrows form by localised de‐adhesion at small foci at the nascent intersomitic planes, which are consolidated by coalescence of such areas by de‐adhesion to produce the interface. It is not possible to predict precisely where cells would initiate de‐adhesion since there is a stochastic element to the phenomenon. Once formed, boundaries between somites are stable and provide no opportunity for mixing, except across the first formed furrow, which disintegrates at the 4‐6 somite stage. The first ten somites form at a constant rate of 2.3 somites/hr, during which time we recorded constant relative displacement of the segmental plate against the rostro‐caudally elongating notochord. Unlike teleost epiboly and gastrulation, no large‐scale movements of individual cells can be detected during elaboration of the embryonic axis. © 1994 Wiley‐Liss, Inc.
Cellular invasion and collagen type IX in the primary corneal stroma in vitro
Authors: Cai Cindy X. , Fitch John M. , Svoboda Kathy K. H. , Birk David E. , Linsenmayer Thomas F. 
Published: February 2005

AbstractDuring different stages in the development of the avian cornea, various collagen types have been shown to participate in matrix formation and have been implicated in morphogenesis. One of these is the fibril‐associated collagen type IX. This molecule is present when the primary corneal stroma is in a compact state, but rapidly disappears just prior to stromal swelling and its invasion by mesenchymal cells. The temporospatial pattern of the disappearance of type IX collagen in the developing cornea suggests that this molecule may be involved in stabilizing the primary corneal stromal matrix by interacting either with other type IX collagen molecules or with other matrix components. To explore further whether the removal of type IX collagen is involved in stromal swelling, we have employed an in vitro culture system in which swelling of the primary stroma and mesenchymal cell invasion can be experimentally manipulated by culturing chick corneal explants on a Nuclepore filter support in the presence or absence of an associated lens. We have also examined the effect of exogenously added human recombinant tissue inhibitor of metalloproteinases (TIMP‐1) on the presence of type IX collagen and cellular invasion. When stage 25—26+ corneal explants were cultured with an associated lens, the primary stroma did not swell; immunohistochemically detectable type IX collagen was still present, and mesenchymal cell invasion failed to occur. Conversely, when the same stages of corneal explants were cultured without an associated lens, the primary stroma swelled; type IX collagen disappeared, and mesenchymal cell migration occurred. Under both conditions, however, the type II collagen of the stroma, which is known to be a component of the striated fibrils, remained clearly detectable and with time even seemed to increase in amount. This result is consistent with the proposition that type IX collagen is one factor involved in maintaining the primary stroma as a compact matrix, possibly by functioning as a bridging/stabilizing factor. When TIMP was added to cultures of corneal explants, type IX collagen remained detectable in focal regions, suggesting that one or more metalloproteinases are involved in the removal of the type IX collagen. In addition, some of these type IX‐containing regions contained mesenchymal cells, suggesting that in addition to type IX collagen other factors are likely to be involved in regulating mesenchymal cell migration. © 1994 Wiley‐Liss, Inc.
Expression of epidermal growth factor family gene members in early mouse development
Authors: Johnson Susan E. , Rothstein Jay L. , Knowles Barbara B. 
Published: February 2005

AbstractTranscription of four members of the epidermal growth factor (EGF) family, EGF, TGF‐α, Amphiregulin, and Cripto, was investigated in the ovulated unfertilized egg and preimplantation embryo using cDNA libraries. EGF was present as a maternal message only, TGF‐α was present at low levels in each library, Amphiregulin was not detected, and Cripto transcripts were first detected in the blastocyst cDNA library. In situ hybridization studies of the implanting embryo revealed Cripto expression localized to the entire ectoderm and then to the rapidly growing ectoplacental cone. At gastrulation, Cripto was detected in the primitive streak and developing mesoderm. During organogenesis, Cripto localized to the developing heart. Two Cripto transcripts were detected: one is confined to the early embryo and teratocarcinoma cells, and the other, first found in the fetus, is the major form detected in adult organs. © 1994 Wiley‐Liss, Inc.
Stage‐specific expression of alkaline phosphatase during neural development in the mouse
Authors: Narisawa Sonoko , Hasegawa Hideaki , Watanabe Keiichi , Millán José Luis 
Published: February 2005

AbstractThe expression pattern of tissue nonspecific alkaline phosphatase (TNAP) in the developing neural tube of mouse is reported. Homogeneous AP activity in the neuroepithelium becomes prominent at E8.5. AT E9.5, distinctly AP‐positive cells appear in the brain and spinal cord area. At stages E10.5 to E12.5, AP positivity is observed between the mesencephalon and the rhombencephalon, along the entire spinal cord and cranial nerves emerging from the myelencephalon. At E13.5, strongly AP positive fibers become prominent in the pons. At E14.5, AP expression in brain tissue is considerably reduced and there is a complete absence of AP activity in the nerve cells and glial cells of adult brain. The choroid plexus remains distinctly positive for AP expression until the adult stage. Northern blot analysis and reverse‐transcriptase polymerase chain reaction amplification of RNA indicate that this AP activity results from the expression of the Akp‐2 locus. This AP expression pattern is distinct from those reported for the expression of GD3, nestin, Hox 2.3, and Wnt‐1 during brain development. We conclude that AP is a useful marker of a subpopulation of neuroectodermal cells present in the neural tube as early as E8.5, at which stages there are no other AP positive intraembryonic cells except PGCs. © 1994 Wiley‐Liss, Inc.
Expression of M‐cadherin protein in myogenic cells during prenatal mouse development and differentiation of embryonic stem cells in culture
Authors: Rose Olaf , Rohwedel Jürgen , Reinhardt Sigrid , Bachmann Michael , Cramer Matthias , Rotter Max , Wobus Anna , Starzinski‐Powitz Anna 
Published: February 2005

AbstractMolecules regulating morphogenesis by cell‐cell interactions are the cadherins, a class of calcium‐dependent adhesion molecules. One of its members, M‐cadherin, has been isolated from a myoblast cell line (Donalies et al. [1991] Proc. Natl. Acad. Sci. U.S.A. 88:8024—8028). In mouse development, expression of M‐cadherin mRNA first appears at day 8.5 of gestation (E8.5) in somites and has been postulated to be down‐regulated in developing muscle masses (Moore and Walsh [1993] Development 117:1409—1420). Affinity‐purified polyclonal M‐cadherin antibodies, detecting a protein of approximately 120 kDa, were used to study the cell expression pattern of M‐cadherin protein. It was first visualized in somites at E10 1/3 and could be confined to desmin positive, myotomal cells. At all subsequent prenatal stages, M‐cadherin was only found in myogenic cells of somitic origin. The detection of the protein at E10 1/3 suggests a translational delay of M‐cadherin mRNA of 1 to 2 days (E8.5 vs. E10 1/3). This was further supported by the finding that during differentiation of ES cell line BLC6 into skeletal muscle cells in culture, expression of M‐cadherin mRNA can be detected 2 days prior to M‐cadherin protein. During prenatal development, the pattern of M‐cadherin expression changes: In E10 1/3 embryos and also in myotomal cells of later stages, M‐cadherin is evenly distributed on the cell surface. In developing muscle masses (tested at E16 to E18), however, M‐cadherin protein becomes clustered most likely at sites of cell‐cell contact as indicated by double‐labelling experiments: M‐cadherin‐staining is the positive image of laminin negative areas excluding the presence of a basal lamina at M‐cadherin positive sites. Furthermore, M‐cadherin is coexpressed with the neuronal cell adhesion molecule N‐CAM which has been shown to mediate cell‐cell contact in myogenic cells. In summary, our results are in line with the idea that M‐cadherin might play a central role in myogenic morphogenesis. © 1994 Wiley‐Liss, Inc.
Prospective fate map of the mouse primitive streak at 7.5 days of gestation
Authors: Smith Jodi L. , Gesteland Katherine M. , Schoenwolf Gary C. 
Published: February 2005

AbstractFluorescent dyes were used in the present study to map three rostrocaudal levels of the primitive streak of mouse embryos at 7.5 days of gestation. Injections at the most rostral level, the 1/4 streak level, principally labeled cells of the paraxial mesoderm, including mesenchyme in the head, and somites and segmental plate mesoderm in the trunk. Injections at the intermediate level, the 1/2 streak level, principally labeled cells of the lateral plate mesoderm of the trunk. Injections at the most caudal level, the 3/4 streak level, principally labeled cells of the extraembryonic mesoderm at the periphery (i.e., caudolateral portion) of the embryo adjacent to the developing amnion, yolk sac, and allantois. However, injections placed at all three primitive‐streak levels provided some labeled cells to the areas of the ingressed mesoderm derived from immediately adjacent levels, suggesting that prospective mesodermal areas are not fully spatially segregated from one another at this stage. These data combined with those from a companion study in which the structure of the node was defined and its derivatives were mapped (Sulik et al. [1994] Dev. Dyn. 201:260—278) allowed us to construct a prospective fate map of the mouse primitive streak at 7.5 days of gestation. This map revealed that mediolateral subdivisions of the ingressed mesoderm were arrayed in rostrocaudal sequence within the primitive streak, such that more rostral levels of the streak contained prospective medial cells (e.g., notochord and paraxial mesoderm), intermediate levels contained prospective intermediate cells (e.g., intermediate mesoderm or nephrotome and lateral plate mesoderm), and more caudal levels contained prospective lateromost cells (e.g., extraembryonic mesoderm). Prospective mesodermal cells, with the exception of those of the notochord, ingressed bilaterally from the primitive streak, contributing to the mesoderm on both the right and left sides of the axis. Our prospective fate map of the mouse primitive streak at 7.5 days of gestation, when compared to a map of the avian primitive streak at a comparable stage of development (Schoenwolf et al. [1992] Dev. Dyn. 193:235—248), demonstrates that considerable congruity exists between the locations of mesoderm precursor cells in birds and mammals. Thus, similar morphogenetic movements underlie mesoderm formation during avian and mammalian gastrulation. Moreover, prospective mesodermal locations within the mouse primitive streak correspond to recently described patterns of early gene expression (Sasaki and Hogan [1993] Development 118:47—59; Takada et al. [1994] Genes Dev. 8:174—189; Rossant, personal communication). © 1994 Wiley‐Liss, Inc.
Temporally and spatially restricted expression of apolipoprotein J in the developing heart defines discrete stages of valve morphogenesis
Authors: Witte David P. , Aronow Bruce J. , Dry Jane K. , Harmony Judith A. K. 
Published: February 2005

AbstractDuring cardiac valve morphogenesis, a series of interactions between the mesodermal‐derived myocardium and the overlying endothelium lead to condensed leaflet structure formation. At the atrioventricular (AV) canal, endocardial cells are transformed by specialized underlying myocardial cells into endocardial cushions, and then remodeled into mitral and tricuspid valves. Aortic and pulmonary valves develop by a similar mechanism in the primitive outflow tract. Few genes exhibit restricted spatiotemporal expression in these critical embryonic structures, thus limiting the clues to the sequence of molecular events necessary for valvulogenesis. Apolipoprotein J (ApoJ), a secreted glycoprotein expressed in a variety of cell types at tissue interfaces, exhibits a highly restricted and dynamic expression pattern in the developing heart. ApoJ transcripts were detected in mice at day 9.0 of gestation in the wall of the developing truncus arteriosus. By day 10, intense signal occurred in a thin layer of myocardial cells adjacent to developing endocardial cushions of both atrioventricular canal and truncus arteriosus. No apoJ mRNA was present in the overlying endocardial cushions until day 13.5 when prevalvular condensation begins. Intense expression occurred in the stromal connective tissue throughout leaflet formation. The highly restricted spatiotemporal expression pattern of apoJ in the developing heart implicates its role in the morphogenesis of the AV canal and outflow tract into cardiac valves. © 1994 Wiley‐Liss, Inc.
Influence of digits, ectoderm, and retinoic acid on chondrogenesis by mouse interdigital mesoderm in culture
Authors: Lee Kenneth K. H. , Li Felix C. H. , Young W. T. , Kung Jean L. S. , Ng Jim L. , Cheah Kathryn S. E. 
Published: February 2005

AbstractWe have cultured tissues isolated from the interdigital zones (IDZ) of the mouse footplate in the presence of the digits, ectoderm, and all‐trans retionic acid. The objective was to understand how these various factors influence the developmental fate of the interdigital tissues. Neutral red staining showed that these tissues normally differentiate by dying between day 12.5–14.5. However, if they were isolated from the footplate between day 12.5–13.5 (when cell death is not overtly obvious in the IDZ) and maintained in organ culture, these tissues would develop into cartilage and soft connective tissues. In culture, chondrogenesis is initiated very rapidly in the interdigital explants as revealed by in situ hybridization with riboprobes specific for type IIA and IIB procollagen mRNAs. The ability of interdigital tissues to form cartilage is not attributed to factors present in the serum of the culture medium as this phenomenon is also observed in serumless cultures. We have found that if all‐trans retinoic acid, at concentrations of 10–50 ng/ml culture medium, were added to the explants it could inhibit chondrogenesis and promote cell death. Moreover, in some of the cultures, a single digit was left attached to the interdigital tissue. This also dramatically reduced the incidence of chondrogenesis. We have tried to determine whether the digits and ectoderm can produce a diffusible factor that can prevent cartilage from developing by culturing day 12.5 interdigital tissues in ectoderm and digit conditioned media. The ectoderm conditioned medium had no effects on interdigital growth or chondrogenesis. In contrast, the size of interdigital explants cultured in the presence of digit conditioned medium was shown to be significantly smaller than the control. These explants also produced a smaller quantity of cartilage as revealed by Alcian blue binding assay. In sum, our results showed that the fate of the interdigital tissues are not fully determined until after day 13.5. These tissues have the potentials to form cartilage and soft connective tissues. We tentatively propose that these interdigital tissues do not normally realize their histogenetic potentials because of the antichondrogenic influence of the digits and retinoic acid. © 1994 Wiley‐Liss, Inc.
Insertion of a targeting construct in a Hoxd‐10 allele can influence the control of Hoxd‐9 expression
Authors: Rijli Filippo M. , Dollé Pascal , Fraulob Valérie , LeMeur Marianne , Chambon Pierre 
Published: February 2005

AbstractA neomycin resistance (neo) gene driven by the phosphoglycerokinase (PGK) promoter was inserted into the Hoxd‐10 homeobox by homologous recombination in embryonic stem (ES) cells. Chimeric mice derived from ES cell‐injected blastocysts died shortly after birth. Craniofacial and axial abnormalities were found in the skeleton of these chimeras, resembling some of the previously described Hox gene gain‐of‐function phenotypes. The spatial expression patterns of various Hoxd gene transcripts were analysed in chimeric mutant embryos by in situ hybridization. Two main observations were made: (1) a wide ectopic expression domain of the Hoxd‐9 gene was found in the spinal cord of these embryos, and (2) the neo gene exhibited a specific Hox‐like expression domain which extended far more rostrally than that of the Hoxd‐10 gene, showing that, in the context of this mutation, the PGK promoter could be regulated as a Hox promoter. These results provide the first evidence that a targeted insertion into a Hox gene coding sequence, in the context of its own cluster, could result in misexpression of a neighbour gene of the complex. © 1994 Wiley‐Liss, Inc.
Expression of β1 integrins changes during transformation of avian lens epithelium to mesenchyme in collagen gels
Authors: Zuk Anna , Hay Elizabeth D. 
Published: February 2005

AbstractRemarkably, a number of definitive epithelia, such as that of the anterior lens, give rise when suspended within 3D gels of type I collagen, to elongate, bipolar shaped cells that exhibit the ultrastructure, polarity, and migratory ability of mesenchymal cells. They begin producing type I collagen and stop producing crystallins, type IV collagen, and laminin. Here, we investigated changes in β1 integrins and their extracellular matrix (ECM) ligands during this transdifferentiation. The former free surface of the lens epithelium that is now in contact with collagen begins within a day to stain intensely for β1 and it is this surface rather than the surface facing the basement membrane that gives rise to mesenchymal cells. Immunoprecipitation experiments reveal a large increase in the β1 integrin subunit on mesenchymal cells as compared to the epithelium of origin. The α5 integrin subunit, which is barely detectable in the lens, increases in the mesenchymal cells and α3 continues to be expressed at about the same level as in the epithelium. α6, the epithelial integrin subunit, and laminin, its ECM ligand, are not detected immunohistochemically or biochemically in the mesenchyme. Rather, the mesenchymal cells secrete abundant fibronectin, the major ECM ligand for α5β1. RGD peptides do not inhibit the transformation but antibodies to β1 do perturb the emigration of mesenchymal cells from the lens apical surface. We conclude that the β1 integrins newly expressed on the apical epithelial surface interact with the surrounding 3D collagen gel to help bring about this unusual epithelial‐mesenchymal transition. © 1994 Wiley‐Liss, Inc.
Chondrogenic potential of chick embryonic calvaria: I. Low calcium permits cartilage differentiation
Authors: Jacenko Olena , Tuan Rocky S. 
Published: February 2005

AbstractCalvaria from day‐14 calcium‐deficient chick embryos produced by long‐term maintenance in shell‐less culture, exhibit a cartilage‐like phenotype (Jacenko and Tuan [1986] Dev. Biol. 115:215–232), which is restored to an osteogenic phenotype upon calcium repletion to the embryo. The expression of cartilage markers in a typically osteogenic tissue under calcium deficiency implies the presence of chondrogenic cells, and questions the conditions associated with calcium deficiency which may cause their divergent pathway of differentiation. In the present study, by explanting normal and shell‐less embryonic calvarial pairs in organ culture in vitro and experimentally regulating their calcium supply, the calcium status of the calvaria was modulated as a function of medium calcium. Histological and immunoblotting analyses demonstrated for the first time that calvaria possess cells which can form genuine cartilage. This chondrogenic potential is expressed only in a low‐calcium environment, where cartilage forms in both normal and shell‐less calvarial pairs; their calcium‐suplemented counterparts, however, develop as fully osteogenic tissues. Furthermore, chondrogenesis in both normal and shell‐less calvaria indicates that the chondrogenic cells must be endogenous constituents of the calvaria, rather than being derived elsewhere in response to systemic calcium deficiency. Finally, the correlation between matrix under‐calcification and cartilage expression in the embryonic calvarium suggests that calcium, perhaps in the form of matrix mineral, may modulate cell differentiation during skeletogenesis. © 1995 Wiley‐Liss, Inc.
Chondrogenic potential of chick embryonic calvaria: II. Matrix calcium may repress cartilage differentiation
Authors: Jacenko Olena , Antonio James D. San , Tuan Rocky S. 
Published: February 2005

AbstractChick embryos cultured in the absence of their eggshell are rendered severely calcium‐deficient, and develop a cartilage‐like phenotype in the calvarium, a normally osteogenic tissue. In the preceding paper (Jacenko and Tuan [1995] Dev. Dyn. 202:13–26), experiments using organ cultured calvaria from day‐12 normal and shell‐less embryos showed that depletion of calcium alone may be responsible in promoting chondrogenic differentiation in calvaria. Here these findings were extended using an in vivo calvarial grafting technique, such that the extent of calvarial matrix calcification was a function of the calcium status of both the graft and the host. In these calvarial grafts, undermineralized regions again were shown to support chondrogenesis. To identify possible mechanisms which promote chondrogenesis in the calvaria, cells were enzymatically dissociated from the calvaria and cultured in media with varied levels of soluble calcium, under conditions which should modulate cell‐to‐cell interactions, including monolayer, micromass, agarose gels, and suspension cultures. Soluble calcium had no effect on calvarial cell differentiation, whereas conditions which enhanced cell‐cell interactions, e.g., suspension culture, elicited cartilage expression. Based on these findings, we propose that the calcified matrix of the calvarium is repressive to chondrogenesis during normal development, but that the lack of mineral in a calcium‐deficient calvarium creates a microenvironment permissive for cell‐to‐cell interactions which lead to chondrogenic differentiation. © 1995 Wiley‐Liss, Inc.