bluuebunny/crossref_metadata_2025_split huggingface dataset:
Distinct regions of human fibronectin are essential for fibril assembly in an in vivo developing system
Authors: Darribére Thierry , Koteliansky Victor E. , Chernousov Michael A. , Akiyama Steven K. , Yamada Kenneth M. , Thiery Jean Paul , Boucaut Jean‐Claude 
Published: February 2005

AbstractIn early vertebrate development, the proper assembly of fibronectin into fibrils is crucial for embryonic cells to adhere and to migrate on the extracellular matrix. The molecular mechanisms by which such a process occurs in vivo are poorly understood. In the amphibian embryo Pleurodeles waltl fibronectin fibrils appear first at the blastula stage. They form a fibrillar matrix on the basal surface of animal cells facing the blastocoel. Using competition and perturbation experiments with purified proteolytic fragments and domain‐specific monoclonal antibodies, we demonstrate that at least three fibronectin sites are essential for assembly of fibronectin fibrils in the blastula of Pleurodeles waltl. Two sites, the RGDS sequence and the synergistic domain in the 10th type III repeat, are both involved in receptor recognition. A third site that spans the 9th type I and 1st type III homology sequences is also likely to participate in fibronectin‐fibronectin interactions. © 1992 Wiley‐Liss, Inc.
A cyclical, developmentally‐regulated death phenomenon in a colonial urochordate
Authors: Lauzon Robert J. , Ishizuka Katherine J. , Weissman Irving L. 
Published: February 2005

AbstractBotryllus schlosseri is a colonial ascidian whose asexually derived, clonally modular systems of zooids exhibit developmental synchrony. The blastogenic cycle culminates in a phase of programmed cell and zooid death called takeover, in which all functional zooids die over a 30 hr period, and are replaced by a new generation of individuals. Because of the weekly recurrence and magnitude of visceral death in this model organism, we have begun to characterize the mechanisms that govern takeover. Here we describe a monoclonal antibody (B3F12.9) that recognizes a novel 57 Kd polypeptide (under reducing conditions) localized to the perivisceral extracellular matrix (PVEM) of buds and zooids, as well as blood cells of Botryllus by immunofluorescence and immunogold labeling of tissue sections. During their active feeding phase, zooids exhibited a uniform labeling pattern of PVEM along their anteroposterior (A‐P) axis. At the onset of takeover (T = 3 hr), B3F12.9 immunostaining became diffuse or absent at the anterior end, which paralleled the axis of contraction of the dying zooid, whereas the posterior end retained its labeling integrity. During mid (T = 15 hr) to late (T = 28 hr) takeover, issue damage was extensive, large blood macrophages and other B3F12.9 immunoreactive blood cells invaded the peribranchial cavity, whereas PVEM labeling gradually disappeared along the entire A‐P axis. These findings indicate that takeover is a dynamic process in which extracellular matrix breakdown proceeds in a polarized fashion, beginning at the anterior end of each zooid and gradually propagating toward the posterior end. © 1992 Wiley‐Liss, Inc.
Coordinated induction of cell proliferation and syndecan expression in dental mesenchyme by epithelium: Evidence for diffusible signals
Authors: Vainio Seppo , Thesleff Irma 
Published: February 2005

AbstractEpithelial–mesenchymal interactions induce the expression of syndecan, a cell surface proteoglycan, and tenascin, an extracellular matrix glycoprotein in the mesenchymal component of many organ rudiments including the tooth. Experimental recombination cultures of early dental epithelium and mesenchyme were analysed by double immunostaining to compare the distribution of syndecan, tenascin, and proliferating cells (BrdU incorporation) in the induced dental mesenchyme. After 5–9 hr in culture expression of syndecan and tenascin as well as an increase in BrdU incorporation were evident in the mesenchymal cells adjacent to the epithelium and the positive area enlarged with time. Syndecan and tenascin were colocalized only partially in some explants. The expression of syndecan and tenascin in the recombinants correlates with their stage‐dependent expression pattern during early tooth development in vivo (Vainio and Thesleff, 1992). The area of increased cell proliferation in the mesenchyme correlated closely with syndecan expression. In none of the explants was increased BrdU incorporation observed in syndecan negative areas. Epithelium induced also condensation of the mesenchymal cells. Induction and spread of the syndecan‐positive zone in the dental mesenchyme required close and continuous contact with the epithelium. The mechanism by which the induction of syndecan expression spreads in the mesenchyme was studied in rat‐mouse interspecies recombination cultures, using syndecan antibodies that recognize mouse but not rat syndecan. The rat mesenchyme and epithelium were first cultured in contact for 24 hr. Then the epithelium was removed and freshly dissected, “uninduced” mouse mesenchyme was placed in contact with different aspects of the rat mesenchyme. The rat mesenchymal cells that had located next to the epithelial tissue stimulated syndecan expression in adjacent mouse mesenchyme. The induction potential was gradually lost toward the periphery of the rat mesenchyme. Based on these findings we suggest that diffusible signal molecules mediate the spread of syndecan induction in the mesenchyme and that syndecan plays a role in the regulation of cell proliferation. © 1992 Wiley‐Liss, Inc.
Localization of type II collagen, long form α1(IX) collagen, and short form α1(IX) collagen transcripts in the developing chick notochord and axial skeleton
Authors: Swiderski Ruth E. , Solursh Michael 
Published: February 2005

AbstractIn this study we compare, by in situ hybridization, the spatial and temporal expression patterns of transcripts of avian type II collagen and the long and short forms of the (α1) chain of type IX collagen during the development of the notochord and axial skeleton. We observed type II collagen and short form type IX collagen transcripts in the developing (stage 25–28) nonchondrogenic notochord. Conversely, long form type IX transcripts were not detectable in the notochord or perinotochordal sheath. Interestingly, all three transcripts colocalized in the developing chondrogenic vertebrae of the axial skeleton as well as in the chondrocranium and Meckel's cartilage. The expression of the short form of type IX collagen in these regions was more restricted than that of the long form. This report provides additional support for a complex regulatory pathway of cartilage marker gene expression in chondrogenic vs. nonchondrogenic tissues during avian embryogenesis. © 1992 Wiley‐Liss, Inc.
Urokinase expression during the epithelial–mesenchymal transformation of the avian somite
Authors: McGuire Paul G. , Alexander Susan M. 
Published: February 2005

AbstractEarly events in the morphogenesis of the axial skeleton involve an epithelial‐mesenchymal transformation of the somites. Cells of the ventromedial wall of the somite (the sclerotome) migrate to regions surrounding the notochord and neural tube and condense to form the cartilage model of the vertebrae. Urokinase activity in the axial region of the quail embryo trunk was found to increase during these stages. In situ hybridization localized urokinase mRNA expression in this region and suggests an important role for this protease in the process of cell migration and matrix remodeling during development of the axial skeleton. © 1992 Wiley‐Liss, Inc.
Neuroblastoma × spinal cord (NSC) hybrid cell lines resemble developing motor neurons
Authors: Cashman Neil R. , Durham Heather D. , Blusztajn Jan Krzysztof , Oda Kenichiro , Tabira Takeshi , Shaw Ivan T. , Dahrouge Simone , Antel Jack P. 
Published: February 2005

AbstractWe have developed a series of mouse‐mouse neural hybrid cell lines by fusing the aminopterin‐sensitive neuroblastoma N18TG2 with motor neuron‐enriched embryonic day 12–14 spinal cord cells. Of 30 neuroblastoma‐spinal cord (NSC) hybrids displaying a multipolar neuron‐like phenotype, 10 express choline acetyltransferase, and 4 induce twitching in cocultured mouse myotubules. NSC‐19, NSC‐34, and their subclones express additional properties expected of motor neurons, including generation of action potentials, expression of neurofilament triplet proteins, and acetylcholine synthesis, storage, and release. In addition, NSC‐34 cells induce acetylcholine receptor clusters on cocultured myotubes, and undergo a vimentin‐neurofilament switch with maturation in culture, similar to that occurring in neuronal development. NSC cell lines appear to model selected aspects of motor neuron development in an immortalized clonal system. © 1992 Wiley‐Liss, Inc.
Id expression during mouse development: A role in morphogenesis
Authors: Wang Yaoqi , Benezra Robert , Sassoon David A. 
Published: February 2005

AbstractWe have characterized the spatial and temporal pattern of Id transcription during mouse embryogenesis. The Id gene encodes a helix–loop–helix (HLH) protein which can heterodimerize with the ubiquitously expressed HLH protein products of the E2A gene, and prevent them from binding DNA either alone or as a heterodimer with tissue specific HLH transcription factors such as the muscle determination gene, MyoD1 (Benezra et al., 1990: Cell 61:49–59). Since Id has been shown to be down‐regulated during induced differentiation in several cell lines, it has been postulated that Id plays a general inhibitory role in cell differentiation (Benezra et al., 1990). In situ analysis of Id mRNA expression in the mouse embryo was performed in order to determine whether the pattern of Id expression is consistent with this postulate. A detailed study throughout the entirety of mouse postimplantation development reveals that Id is expressed upon gastrulation at very high levels in almost all regions of the mouse embryo and expression declines as embryogenesis proceeds. In skeletal muscle, in which the inhibitory action of Id has been established in tissue culture models (Benezra et al., 1990), Id and the HLH myogenic factors are expressed in a mutually exclusive manner suggesting that myogenic precursors do not express both types of HLH gene products. In addition, Id colocalizes both spatially and temporally with Hox‐7.1, a murine homeobox gene which is associated with regions of high cell proliferation and positional fate assignment. © 1992 Wiley‐Liss, Inc.
Retinoic acid receptor β2 mRNA is elevated by retinoic acid in vivo in susceptible regions of mid‐gestation mouse embryos
Authors: Harnish Douglas C. , Jiang H. , Soprano Kenneth J. , Kochhar D. M. , Soprano Dianne Robert 
Published: February 2005

AbstractMany of the biological effects of retinoic acid are mediated by its nuclear receptors (RAR‐α, RAR‐β, and RAR‐γ), and each of these three receptors exist in multiple isoforms. As a first step to identify if any of the receptor isoforms are involved in dysmorphogenesis which is induced in mouse embryos after treatment with retinoic acid (RA), we examined the levels of mRNA of several isoforms of each RAR in the limb buds and other embryonic regions of normal and RA‐treated embryos. Within 3 to 6 hr after treatment of mice on day 11 of gestation with RA, RAR‐β2 mRNA levels in the whole embryo increased 7‐fold while both RAR‐α2 and RAR‐γ1 mRNA levels were elevated only 2‐fold. Since RA treatment of day 11 embryos especially produces limb defects in virtually every embryo, we next examined individual embryonic regions separately. Limb buds showed the highest elevations in RAR‐β2 mRNA levels (12‐fold) compared to a moderate elevation in the head/craniofacial region (8‐fold) and a small elevation in the remainder of the body (4‐fold). In contrast, RAR‐α2 and RAR‐γ1 mRNA levels were elevated in all these tissues to a similar extent, which amounted to only about a 2‐fold increase. Retinol, the precursor of RA in the embryo, was also capable of elevating RAR‐β2 mRNA levels in the limb bud, but the increase was delayed, apparently indicating that metabolic conversion of retinol to RA preceded the effect on mRNA levels. Finally, treatment of dams on day 14 of gestation, a time when embryos are relatively insensitive to RA, resulted in no elevation in RAR‐α2 mRNA levels and a greatly reduced elevation (2‐ to 3‐fold in all embryonic regions) in RAR‐β2 mRNA levels. Therefore, the elevation in RAR‐β2 mRNA correlates well with regions of the embryo, e.g., limb buds, which are specific targets for RA‐induced teratogenesis. These results are consistent with the possibility that specific isoforms of the RARs, in particular RAR‐β2, may mediate the effects of RA during abnormal development. © 1992 Wiley‐Liss, Inc.
Proteoglycans and the modulation of cell adhesion by steric exclusion
Authors: Morris John E. 
Published: February 2005

AbstractThe hypothesis that cell aggregation may be driven by linear polymers in the matrix, particularly glycosaminoglycans, is revisited in light of more recent evidence. A model is proposed that extends the concept of steric exclusion to include a role in determining the directionality of cell migration and neurite extension. Recent literature is reviewed to support the conclusion that in living tissues the theoretical conditions for driving aggregation and migration by steric exclusion are met. The ability of a linear polymer to exclude cells is a function of its viscosity, which is optimum with glycosaminoglycans similar to chondroitin sulfate. It is ineffective with low viscosity glycosaminoglycans such as most heparin or heparan sulfate. Hyaluronic acid, a massive polymer, excludes cells poorly when present as an open matrix gel but forms an effective exclusion barrier when attached to the cell surface. According to a model for steric exclusion in organogenesis, when cells have a glycocalyx of linear polymer, they should disperse and migrate down a viscosity gradient of excluding matrix polymer; when they shed or internalize their surface coat in the continued presence of matrix, they should be excluded into a smaller volume and thus stimulated to aggregate. © 1993 wiley‐Liss, Inc.
5A11 antigen is a cell recognition molecule which is involved in neuronal‐glial interactions in avian neural retina
Authors: Fadool James M. , Linser Paul J. 
Published: February 2005

AbstractIn continuing efforts to identify cell‐surface molecules involved in cell‐cell interactions in the developing avian retina, we identified a monoclonal antibody, the 5A11 antibody, which possessed the ability to interfere with contact‐dependent glial cell maturation in vitro. We sought to determine the molecular and biochemical identity of the glycoprotein recognized by this antibody, and using additional criteria, establish whether the 5All antigen is indeed a cell‐recognition molecule in the developing retina. Immuno‐histochemical analyses demonstrate that in the hatchling chick retina and in live cultures of embryonic retina cells, the 5A11 antigen is predominantly associated with Müller glial cells whereas little is observed on neuronal elements. Microsequencing of the major component isolated by immunoaffinity chromatography identifies the HT7 antigen (Seulberger et al.: EMBO Journal 9:2151–2158, 1990), a unique member of the immunoglobulin super gene family (IGSF), as a homologous if not identical protein to the 5A11 antigen. The HT7 antibody, furthermore, recognizes affinity purified 5A11 antigen, and both the HT7 antibody and additional probes generated against the 5A11 antigen recognize a major polypeptide of 45.5 kDa and a minor band of 69 kDa on Western blots of membrane preparations from neural retina. To verify that the 5A11 antigen mediates cell‐cell recognition events in the developing neural retina, we examined the consequences of adding antibody to monolayer cultures of dissociated embryonic retina cells and to dissociated retina cells in rotation‐mediated suspension culture. Addition of the 5A11 antibody to monolayer cultures results in alteration in the development of the stereotypic arrangement of neurons and glia characterized by a reduction in the number and complexity of neural extensions upon the glial‐derived flat cells. Similarly, addition of antibodies generated against the 5A11 antigen to dissociated cells in rotation cultures significantly reduces retina cell reaggregation as monitored by computer‐assisted image analysis of cell aggregate size. These data and the identification of the 5A11 antigen as a member of the IGSF establish a role for the 5A11 antigen as a novel recognition molecule in the developing neural retina. © 1993 wiley‐Liss, Inc.
Region‐specific patterns of beta keratin expression during avian skin development
Authors: Knapp L. W. , Shames R. B. , Barnes G. L. , Sawyer R. H. 
Published: February 2005

AbstractThe transient embryonic layers primarily composed of a periderm and subperiderm cover most regions of the chick embryo and are the first suprabasal cell layers covering the body ectoderm. This study presents evidence for regional vriation in the expression of beta keratin in the embryonic layers. Here we show that the embryonic layers covering the anterior metatarsal region of the chicken hindlimb (scutate scale forming region) produce several members of the beta keratin family of polypeptides, designated beta (β) 1–7. These specific polypeptides are later expressed in this region exclusively in the thick, cornified beta strata of mature scutate scales. In contrast to this sequence of events, the embryonic layers overlying the epidermis of the ventral foot pad (reticulate scale‐forming region) and those covering the epidermis in apteric regions of the body produce beta keratin polypeptides β1–3 and β2,3, respectively, but no subsequent expression of these proteins occurs in the mature epidermises of these regions. Furthermore, we find that the embryonic layers of the skin overlying the anterior metatasal region of birds homozygous for the mutation “scaleless” (sc/sc), which completely lack scutate scales, produce the same members of the beta keratin family, β1–7, as the embryonic layers and beta strata of normal scutate scales.Thus, the accumulation of specific beta keratin polypeptides in the developing anterior metatarsal region appears to occur in two distinct phases; first, an early region‐specific expression in cells of the embryonic layers followed by a second phase of expression which occurs in conjunction with appendage morphogenesis. The relationship between differentiation of embryonic skin and the expression of beta keratins is discussed. © 1993 wiley‐Liss, Inc.
Spatio‐temporal distribution of acidic and basic FGF indicates a role for FGF in rat lens morphogenesis
Authors: de Iongh R. , McAvoy J. W. 
Published: February 2005

AbstractAs part of an investigation into the role FGF in lens development, we have studied the distribution of both aFGF and bFGF during eye morphogenesis from embryonic days 10 to 18 (E10–E18) in the rat. For aFGF, reactivity was found only in ectoderm at E10, prior to contact between the optic vesicle and presumptive lens ectoderm. During lens placode formation (E11) there was a transient, diffuse reactivity for aFGF in anterior optic vesicle cells directly apposed to the labelled ectoderm of the lens placode. At E12 the diffuse reactivity of the lens placode had changed to a discrete localisation along the basolateral surfaces of differentiating cells in the lens pit. Similar reactivity was associated with neuroblasts along the inner margin of the optic cup. At the early lens vesicle stage (E13) the baso‐lateral aFGF‐like reactivity associated with elongating lens cells was more intense and extensive. From the late lens vesicle stage (E14) to E18, reactivity in the lens was increasingly restricted to the equatorial regions which incorporate the germinative and transitional zones. From E16 to E18, aFGF‐like reactivity in the retina was predominantly localised in the peripheral regions corresponding to the developing ciliary body and iris and in the central retina associated with ganglion cell axons. For bFGF, weak reactivity was detectable as early as E13 in the developing lens capsule and increased in intensity during lens development with the posterior capsule reacting more intensely than the anterior capsule. Retinal bFGF‐like reactivity was first detected at E14, associated with differentiating ganglion cells in the central retina. From E16 to E18 the retinal ganglion cells showed increasing reactivity and the pattern of reactivity followed the centro‐peripheral pattern of retinal development. Thus reactivity for aFGF is first detected in presumptive lens ectoderm and subsequently in optic vesicle cells which are closely associated with lens ectoderm. This raises the possibility that aFGF may be involved in inductive interactions between presumptive lens ectoderm and optic vesicle. Furthermore the localisation patterns established for both aFGF and bFGF during lens and retina morphogenesis suggest an important role for FGF in regulating their morphogenesis and growth. © 1993 Wiley‐Liss, Inc.
Modulation of contractile protein gene expression in fetal murine crural muscles: Emergence of muscle diversity
Authors: Ontell Martin P. , Sopper Maggie M. , Lyons Gary , Buckingham Margaret , Ontell Marcia 
Published: February 2005

AbstractThe modulation of contractile protein gene expression in mouse crural muscles (i.e., muscles located in the region between the knee and ankle) during the fetal period (defined as 15 days gestation to birth), resulting in diversity among and within these muscles, has been evaluated with in situ hybridization and correlated with morphogenetic events in the extensor digitorum longus and soleus muscles. During the fetal period extensive secondary myotube formation occurs in the crural muscles, and the myotubes become innervated (Ontell and Kozeka [1984a, b] Am. J. Anat. 171:133–148, 149–161; Ontell et al. [1988a, b] Am. J. Anat. 181:267–278, 181:278–288). At 15 days gestation, hybridization with 35S‐labeled antisense cRNA probes demonstrates the accumulation of transcripts forα‐cardiac andα‐skeletal actin; MLC1A, MLC1F, and MLC3F; and MHCemb, MHCpn, and MHCβ/slow. At 16 days gestation, accumulation of MHCemb transcripts is reduced (as compared with earlier developmental stages); intensity of signal following hybridization with the probe forα‐skeletal actin is, for the first time, equal to that for the cardiac isoform; and MLC1V mRNA accumulation is discernible. At this stage, variation in transcript accumulation for some mRNAs among and within crural muscles becomes evident. Two factors may play a role in the selective distribution of these transcripts: (1) the stage of muscle maturation; and (2) the future myofiber type. At 16 days gestation anterior crural muscles (which mature ˜ 2 days before posterior crural muscles; Ontell and Kozeka [1984a, b], ibid., Ontell et al. [1988a, b], ibid.) exhibit a greater accumulation of transcripts forα‐skeletal actin and for MLC3F than is found in posterior crural muscles. In muscles that in the neonate are composed, in large part, of slow myofibers, MHCβ/slow and MLC1V mRNAs accumulate in greater amounts, whereas MHCpn transcripts are less abundant in the soleus muscle than in other crural muscles. By 19 days gestation regionalization of transcript accumulation is more pronounced. The soleus muscle, a predominantly slow twitch muscle in the newborn mouse (Wirtz et al. [1983] J. Anat. 137:109–126) exhibits strong signal after hybridization with probes specific for MHCβ/slow and MLC1V. While the level of transcript accumulation for the developmetal isoforms, MHCemb, MLC1A, andα‐cardiac actin, is greatly reduced in most crural muscles at 19 days gestation, these transcripts persist in the soleus muscle at levels equal to or exceeding their amount in limb muscles of 13 day gestation mouse embryos. By 19 days gestation both MyoD and myogenin are “down‐regulated” (as compared with their expression at earlier developmental stages) in all muscle masses. Alterations in contractile protein gene expression are correlated with changes in the myogenic regulatory factors present in fetal hindlimbs during development. © 1993 Wiley‐Liss, Inc.