journal article
LitStream Collection
Home
Fong, Guo‐Hua; Klingensmith, John; Wood, Clive R.; Rossant, Janet; Breitman, Martin L.
doi: 10.1002/(SICI)1097-0177(199609)207:1<1::AID-AJA1>3.0.CO;2-Mpmid: 8875071
Flt‐1 is a high affinity binding receptor for the vascular endothelial cell growth factor (VEGF) and is primarily expressed in endothelial cells. In this study we have investigated the temporal and spatial regulation of its expression by establishing mouse lines containing the lacZ gene targeted into the flt‐1 locus through homologous recombination in embryonic stem (ES) cells. In the yolk sac as well as in the embryo proper, lacZ expression faithfully reflected the endogenous expression pattern of the flt‐1 gene. LacZ staining of heterozygous embryos led to the following observations: (1) the onset of flt‐1 expression is detected at the early primitive streak stage in the extraembryonic mesoderm, and is strongly up‐regulated thereafter, reaching a maximum by early to midsomite stages and declining subsequently; (2) while flt‐1 is widely expressed within the developing vascular endothelium, its expression level is differentially regulated both spatially and temporally. The pattern of flt‐1 expression suggests that it may play an important role in the initiation of endothelium development; and (3) flt‐1 is expressed in essentially all the cells in early blood islands, but later its expression is gradually restricted to the endothelial lineage. Our results indicate that flt‐1 is a marker for hemangioblasts, the presumed progenitor for both hematopoietic and angioblastic lineage. The flt‐1 expression pattern also suggests that it may play important roles in both vasculogenesis and angiogenesis. © 1996 Wiley‐Liss, Inc.
Matzner, Ulrich; Hille‐Rehfeld, Annette; Figura, Kurt Von; Pohlmann, Regina
doi: 10.1002/(SICI)1097-0177(199609)207:1<11::AID-AJA2>3.0.CO;2-Zpmid: 8875072
In mammals, the sorting of newly synthesized lysosomal enzymes is accomplished by two mannose 6‐phosphate receptors (MPR) designated MPR46 and MPR300. MPR300 has an additional function in clearing the nongly‐cosylated insulin‐like growth factor II (IGFII). The distinct expression pattern of the two MPR has been ascribed to the control of MPR300 expression by IGFII. In lower vertebrates, such as chickens or frogs, only MPR300 homologues have been described. These MPR300 homologues do not bind IGFII. In the present study, we examined whether lower vertebrates such as chickens also express two types of MPR and, if so, whether the expression pattern is distinct or similar. We were able to clone chicken cDNA fragments homologous to mammalian MPR46 and MPR300 and to show the synthesis of respective MPR polypeptides, thus establishing the existence of two types of MPR also in a nonmammalian species. Further, we analyzed the expression of the two MPR in chicken by Northern blotting and in situ hybridization. High levels of MPR46 and MPR300 RNA were detectable in epithelia, ganglia, and uropoietic system of chicken embryos. In a number of embryonic and adult tissues, varying ratios of MPR46 and MPR300 RNA were observed. The expression pattern for both MPR46 and MPR300 was distinct, although less pronounced than in mice. We conclude that functional differences unrelated to the additional function of the mammalian MPR300 as a receptor clearing IGFII are responsible for the distinct expression of the two MPR in nonmammalian, and probably also in mammalian, species. © 1996 Wiley‐Liss, Inc.
Niu, Shi; Antin, Parker B.; Akimoto, Kaoru; Morkin, Eugene
doi: 10.1002/(SICI)1097-0177(199609)207:1<25::AID-AJA3>3.0.CO;2-Ypmid: 8875073
An avian cDNA homologue of human and rat glypicans has been cloned from a stage 17 chicken heart cDNA library and used to analyze the distribution of this proteoglycan during development by Northern analysis and whole mount in situ hybridization. At stages 7–12, strong signals were detected in the cephalic region of the neural folds, rostral portion of paraxial mesoderm, and newly formed epithelial somites. At stages 20–25, strong expression was observed in the mantle zone of the telencephalon, the apical epidermal ridge and proximal region of developing limb. Transcripts also were found in the truncus arteriosus and arteriovenous‐canal region of the heart, but not in the myocardium. This distribution pattern suggests that the avian glypican may be involved in the morphogenesis of limb, somite, heart, and brain. The expression of glypican also overlaps FGFs in limb bud, FGF receptors in heart and somite, and NGF receptors in forebrain. The affinity of heparan sulfate proteoglycans for growth factors and the distribution of the avian glypican are consistent with a role for this molecule in growth factor‐mediated signals. © 1996 Wiley‐Liss, Inc.
Hoyle, Christine; Henderson, Deborah J.; Matthews, David J.; Copp, Andrew J.
doi: 10.1002/(SICI)1097-0177(199609)207:1<35::AID-AJA4>3.0.CO;2-Xpmid: 8875074
The iron‐binding growth factor transferrin is taken up and localised in the hindgut of midgestation mouse embryos. We investigated whether the distribution of transferrin may be disturbed in mutant curly tail embryos, a proportion of which exhibit a cell proliferation defect affecting the hindgut endoderm, as part of the pathogenetic sequence leading to development of neural tube defects. Immunostaining revealed a reduction in the binding and/or uptake of transferrin by hindgut epithelial cells in affected curly tail embryos compared with their unaffected littermates. There was no apparent difference between the two embryo types, however, in the distribution or level of expression of the transferrin receptor. The receptor is expressed specifically in the hindgut endoderm of the 10.5‐day embryo, although its mRNA is present in all tissues of the posterior neuropore region, suggesting posttranscriptional control of gene expression. These findings may indicate a role for transferrin binding and/or uptake in the regulation of cell proliferation in the hindgut endoderm, with a defect in this process in the curly tail mutant. However, an alternative explanation is suggested by our finding that transferrin immunostaining is more intense in the hindgut of unaffected curly tail embryos than in nonmutant CBA/Ca and CD‐1 embryos. Thus, mutant embryos may increase their uptake of transferrin in an attempt to compensate for defective cell proliferation in the hindgut resulting from a defect in another pathway. Only a proportion of embryos are able to mount this compensatory response leading to the observed partial penetrance of developmental defects in the curly tail mutant mouse. © 1996 Wiley‐Liss, Inc.
Hierck, Beerend P.; Gittenberger‐De Groot, Adriana C.; Iperen, Liesbeth Van; Brouwer, Antje; Poelmann, Robert E.
doi: 10.1002/(SICI)1097-0177(199609)207:1<39::AID-AJA5>3.0.CO;2-Xpmid: 8875079
Using immunohistochemical techniques as well as in situ hybridization we were able to elicit the expression pattern of the β4 integrin subunit in the murine heart during development. We show that β4 is not expressed in the heart before E13 and is afterwards restricted to the endocardium of the atrioventricular canal, the outflow tract, and the venous valves in the right atrium. As these are all sites of high shear stress in the heart, we propose a role for α6β4 in the tight adhesion of the endocardial cells to their basement membranes in these segments. Moreover, mouse embryos were treated with all‐trans retinoic acid, which was previously shown to induce congenital malformations, among which malformations of the heart. We show an advanced expression without ectopic localization of cardiac β4 after the administration of retinoic acid. This advanced appearance of β4 was also shown in extracardiac tissue like migrating neural crest cells. Several hypotheses on the mechanism of β4 up‐regulation and a possible role for α6β4 in the development of heart malformations after the administration of retinoic acid are discussed. © 1996 Wiley‐Liss, Inc.
Cardoso, Wellington V.; Mitsialis, S. Alex; Brody, Jerome S.; Williams, Mary C.
doi: 10.1002/(SICI)1097-0177(199609)207:1<47::AID-AJA6>3.0.CO;2-Wpmid: 8875075
Exogenous retinoids alter pattern formation and differentiation in many developing systems, such as limb, vertebrae, and central nervous system. Many of these effects are mediated by changes in expression of patterning genes such as Hox genes and Sonic hedgehog. We have previously shown that exogenous retinoic acid, administered to the embryonic rat lung in culture alters the structural pattern of the developing lung, suppressing formation of distal lung and favoring growth of proximal tubules. To determine whether these retinoic acid‐induced changes in lung development were linked to alterations in pattern‐related genes, we characterized the expression of Hoxa‐2, Hoxb‐6, and Sonic hedgehog mRNAs in vivo and in vitro, with or without 10‐5M retinoic acid, by in situ hybridization and quantitative polymerase chain reaction. Each of these genes demonstrated unique timing and distribution of expression that was similar in vivo and in control cultured embryonic lungs. Hoxb‐6 and Sonic hedgehog mRNAs both decreased during lung development in vivo or in vitro. From the patterns of mRNA expression we propose that Hoxb‐6 is involved in distal airway branching while Hoxa‐2 is involved in differentiation of proximal mesenchymal derivatives and vasculogenesis in the lung. RA upregulated all three genes, changing their developmental pattern of distribution and preventing the developmental decrease in Sonic hedgehog expression. We propose that RA acts to maintain high levels of expression of these and likely other pattern‐related genes in a fashion that is characteristic of the immature lung, promoting continued formation of proximal lung structures and preventing formation of typical distal lung structures of the mature lung. © 1996 Wiley‐Liss, Inc.
Wu, Jianxin; Pines, Mark; Gay, Carol V.; Hurwitz, Shmuel; Leach, Roland M.
doi: 10.1002/(SICI)1097-0177(199609)207:1<69::AID-AJA7>3.0.CO;2-Upmid: 8875077
Osteonectin is an acidic calcium‐binding protein found in cartilage, bone matrix, vascular endothelium, and areas of tissue repair. Using immunocytochemistry, osteonectin has been localized in all zones of the normal avian epiphyseal growth plate with notably high amounts in the hypertrophic zone. In the proximal portion of this zone the staining was intracellular, while in the distal calcifying portion of the hypertrophic zone staining was both intracellular and extracellular. Osteonectin was also detected in the growth plate associated with lesions of chickens with tibial dyschondroplasia (TD). Intense intracellular staining was observed in hypertrophic chondrocytes proximal to the lesion; staining was markedly diminished in the TD lesion; extracellular matrix was devoid of staining. Staining intensity was high along the peripheral edges of the lesion that were undergoing vascularization and resorption. This was the only area in the dysplastic cartilage where staining was observed in the extracellular matrix as well as intracellularly. Similar patterns were viewed in all TD lesions examined, whether they were spontaneous or induced by dietary treatments or genetic selection. © 1996 Wiley‐Liss, Inc.
Haynes, John I.; Duncan, Melinda K.; Piatigorsky, Joram
doi: 10.1002/(SICI)1097-0177(199609)207:1<75::AID-AJA8>3.0.CO;2-Tpmid: 8875078
In order to study the spatial and temporal activity of the mouse αB‐crystallin/small heat shock gene promoter during embryogenesis, we generated mice harboring a transgene consisting of approximately 4 kbp of αB‐crystallin promoter sequence fused to the Escherichia coli lacZ reporter gene. β‐galactosidase activity was first observed in the heart rudiment of 8.5 days post coitum (d.p.c.) embryos. An identical expression pattern was obtained for the endogenous αB‐crystallin gene by whole mount in situ hybridization. At 9.5 d.p.c., β‐galactosidase activity was detected in the lens placode, in the myotome of the somites, in Rathke's pouch (future anterior pituitary), and in some regions of oral ectoderm. We also examined the stress inducibility of the αB‐crystallin promoter in vivo. Injection of sodium arsenite into mice resulted in increased endogenous αB‐crystallin expression in the adrenal gland and possibly the liver. Our results indicate that visualization of β‐galactosidase activity provides an accurate reflection of endogenous αB‐crystallin expression and demonstrate that the complex developmental pattern of mouse αB‐crystallin gene expression is regulated at the transcriptional level. This expression pattern, coupled with the present literature which addresses functions of the protein, suggests a role for the αB‐crystallin/small heat shock protein in intermediate filament turnover and cellular remodeling which occur during normal development and differentiation. © 1996 Wiley‐Liss, Inc. This article is a US Government work and, as such, is in the public domain in the United States of America.
Nicolas, Nathalie; Gallien, Claude L.; Chanoine, Christophe
doi: 10.1002/(SICI)1097-0177(199609)207:1<100::AID-AJA9>3.0.CO;2-Mpmid: 8875076
We have analyzed in adult Xenopus laevis, using in situ hybridization, the spatial and temporal expression patterns of MyoD, myogenin, and α‐skeletal actin and fast myosin heavy chain mRNAs during muscle regeneration following cardiotoxin injury. MyoD transcripts could be detected in the satellite cells as early as the first stage of regeneration and were expressed persistently throughout the regeneration process. Myogenin mRNAs were transiently expressed in forming myotubes. α‐Skeletal actin and fast myosin heavy chain mRNAs were detected precociously, before the young myotube stage. This work has shown, for the first time, the presence of myogenin transcripts during Xenopus myogenesis. © 1996 Wiley‐Liss, Inc.
Showing 1 to 10 of 13 Articles