bluuebunny/crossref_metadata_2025_split huggingface dataset:
Desmosome biogenesis in the mouse preimplantation embryo
Authors: Fleming Tom P. , Garrod David R. , Elsmore Andrew J. 
Published: April 2021

ABSTRACT
The molecular processes underlying the formation of the first desmosomes in the mouse early embryo have been examined by immunocytochemical and biochemical techniques using antibody probes recognising desmosomal proteins 1 and 2 (dp1+2, desmoplakins), dp3 (plakoglobin), desmosomal glycoprotein 1 (dgl, desmoglein) and dg2+3 (desmocollins). Immunofluorescence labelling of staged intact embryos and synchronised cell clusters indicates that dp1+2, dgl and dg2+3 are first detectable on the lateral membrane contact sites between trophectoderm cells in early cavitating blastocysts, coincident with the onset of desmosome formation as seen in ultrastructural preparations. Membrane localisation of these antigens is predominantly punctate in appearance, occurs after division to the 32-cell stage and appears to be coincident with blastocoele formation since non-cavitated embryos/cell clusters of equivalent age/ cell cycle are usually unlabelled. In contrast, dp3 is first detectable at the 32-cell stage at all internal membrane contact sites (including those with inner cell mass cells) in a continuous linear pattern, and appears in both cavitated and non-cavitated specimens. Subsequently during blastocyst expansion, dp3 localisation becomes punctate and restricted to trophectodermal membranes. Immunoprecipitation of desmosomal antigens following metabolic labelling indicates that synthesis of dp3 is underway from at least compaction in the 8-cell embryo, while dp1 + 2 synthesis is first evident in 16-cell morulae. Synthesis of dgl and dg2+3 is not detectable until the early blastocyst stage. These results suggest that desmosome biogenesis in the preimplantation embryo might be regulated by transcription or translation of desmosomal glycoproteins and by maturational changes in the trophectoderm layer associated with blastocoele formation. The earlier expression and wider distribution of dp3 at cell contact areas may reflect non-desmosomal sites (eg, adherens junctions) for this protein and a possible role for dp3 in the development of intercellular junctions.
Tenascin M
r 220000 isoform expression correlates with corneal cell migration
Authors: Kaplony Angelika , Zimmermann Dieter R. , Fischer René W. , Imhof Beata. , Odermatt Bernhard F. , Winterhalter Kaspar H. , Vaughan Lloyd 
Published: April 2021

ABSTRACT
The three isoforms of chicken tenascin, an extracellular matrix glycoprotein, are generated by alternatively spliced fibronectin type III domains. The resulting proteins migrate as bands of MT 220000 (ten220), Mr 200000 (ten200) and Mr 190000 (tenl90) on SDS-PAGE. We describe here two monoclonal antibodies, one specific for ten220 (mAb T17) and another that recognizes all isoforms (mAb T16). These were used to examine the differential expression of isoforms during development.
Most impressive is the close correlation between ten220 expression and cell migration in the embryonic cornea. Initially (stage 18), tenl90/200 can be detected within the corneal epithelium and along the basement membranes of the lens and sclera. Ten220 appears within the primary stroma immediately prior to the invasion by neural-crest-derived cells. This expression is maintained during the subsequent migration of fibro blasts from the conjunctiva into the primary stroma. With the completion of migration and the marked increase in matrix synthesis by corneal fibroblasts, ten220 disappears. Tenl90/200 remains in the region adjoining the endothelium, the Bowman’s membrane and the adjacent stroma. The cell-migration-associated isoform is isolated from extracts of embryonic tissues as a homohexamer. Low molecular weight forms appeared absent but a new tenascin band of Mr 210 000 could be detected in brain extracts which may be a new isoform. We conclude that the synthesis of tenascin isoforms is under tight developmental control and speculate that a function of the additional domains is to facilitate cell migration.
Gradient fields and homeobox genes
Authors: Robertis Eddy M. De , Morita Elaine A. , Cho Ken W. Y. 
Published: April 2021

ABSTRACT
We review here old experiments that defined the existence of morphogenetic gradient fields in vertebrate embryos. The rather abstract idea of cell fields of organforming potential has become less popular among modern developmental and molecular biologists. Results obtained with antibodies directed against homeodomain proteins suggest that gradient fields may indeed be visualized at the level of individual regulatory molecules in vertebrate embryos.
Cell-fate determination in the developing Drosophila eye: role of the rough gene
Authors: Heberlein Ulrike , Mlodzik Marek , Rubin Gerald M. 
Published: April 2021

ABSTRACT
The homeobox-gene rough is required in photoreceptor cells R2 and R5 for normal ommatidial assembly in the developing Drosophila eye. We have used several cell-type-specific markers and double mutant combinations to analyze cell-fate determination in rough. We show that the cells that would normally become R2 and/or R5 express a marker, a lacZ insertion in the seven-up (svp) gene, which is indicative of the Rl/3/4/6 cell fate. In addition, the analysis of mitotically induced svp,ro double mutant clones in the eye indicates that in rough all outer photoreceptors are under the genetic control of the svp gene. These results show that, in the absence of rough function, R2 and R5 fail to be correctly determined and appear to be transformed into cells of the R3/4/1/6 subtype. This transformation and the subsequent developmental defects do not preclude the recruitment of R7 cells. However, the presence of ommatidia containing more than one R7 and/or R8 cell in rough implies a complex network of cellular interactions underlying cell-fate determination in the Drosophila retina
Specification of neurepithelium and surface epithelium in avian transplantation chimeras
Authors: Schoenwolf Gary C. , Alvarez Ignacio S. 
Published: April 2021

ABSTRACT
Previous studies of the avian blastoderm have revealed that extensive displacements occur within the epiblast during gastrulation and neurulation. The present study had two main purposes: (1) to map the origin and movement of prospective surface epithelial cells, and (2) to ask whether neurepithelial and surface epithelial cell fates are determined prior to cell movement, or whether they arise later as a result of the ultimate position attained by cells through their movement. Our results show that the rostral and lateral intraembryonic and extraembryonic surface epithelium originates as far laterally as at the area pellucida-area opaca interface of the early epiblast. Intraembryonic surface epithelial cells rearrange relative to one another, extending medially to contribute to the formation of the neural folds, whereas extraembryonic surface epithelial cells maintain their lateral positions, spreading uniformly as the epiblast expands. Our results further show that surface epithelial and neurepithelial cell fates are labile at the onset of neurulation, suggesting that cell fate is specified following cell movement.
Polyclonal origin of pancreatic islets in aggregation mouse chimaeras
Authors: Deltour L. , Leduque P. , Paldi A. , Ripoche M. A. , Dubois P. , Jami J. 
Published: April 2021

ABSTRACT
In the present study, we have examined the origin and growth pattern of the β cells in pancreatic islets, to determine whether a single progenitor cell gave rise to all the precursors of the islets, or if each of a few progenitor cells is the founder of a different islet, or if each islet is a mixture of cells originating from a pool of progenitor cells. Aggregation mouse chimaeras where the pancreatic β cells derived from each embryo can be identified in the islets on histological sections were analyzed. In two chimaeras, all the islets contained cells from both the aggregated embryo. This clearly demonstrates that each islet resulted from several independent cells. In addition, the β cells derived from either embryo component were in very small clusters in the islets, suggesting that in situ cell division did not account significantly for islet growth.
Migrating neural crest cells in the trunk of the avian embryo are multipotent
Authors: Fraser Scott E. , Bronner-Fraser Marianne 
Published: April 2021

ABSTRACT
Trunk neural crest cells migrate extensively and give rise to diverse cell types, including cells of the sensory and autonomic nervous systems. Previously, we demonstrated that many premigratory trunk neural crest cells give rise to descendants with distinct phenotypes in multiple neural crest derivatives. The results are consistent with the idea that neural crest cells are multipotent prior to their emigration from the neural tube and become restricted in phenotype after leaving the neural tube either during their migration or at their sites of localization. Here, we test the developmental potential of migrating trunk neural crest cells by microinjecting a vital dye, lysinated rhodamine dextran (LRD), into individual cells as they migrate through the somite. By two days after injection, the LRD-labelled clones contained from 2 to 67 cells, which were distributed unilaterally in all embryos. Most clones were confined to a single segment, though a few contributed to sympathetic ganglia over two segments. A majority of the clones gave rise to cells in multiple neural crest derivatives. Individual migrating neural crest cells gave rise to both sensory and sympathetic neurons (neurofilament-positive), as well as cells with the morphological characteristics of Schwann cells, and other non-neuronal cells (both neurofilament-negative). Even those clones contributing to only one neural crest derivative often contained both neurofilament-positive and neurofilament-negative cells. Our data demonstrate that migrating trunk neural crest cells can be multipotent, giving rise to cells in multiple neural crest derivatives, and contributing to both neuronal and non-neuronal elements within a given derivative. Thus, restriction of neural crest cell fate must occur relatively late in migration or at the final sites of neural crest cell localization.
Quantitative analysis of protein synthesis in mouse embryos. I. Extensive reprogramming at the one- and two-cell stages
Authors: Latham Keith E. , Garrels James I. , Chang Cecile , Solter Davor 
Published: April 2021

ABSTRACT
A quantitative, high-resolution, two-dimensional gel protein database has been constructed for the mouse embryo. This database has been used to obtain a detailed accounting of the amount and relative timing of changes in protein synthesis that occur during the 1-, 2-, and 4-cell stages along with a description of the most prevalent developmentally regulated patterns of synthesis. We find that during these early stages of development the pattern of proteins synthesized changes to a much greater extent than previously appreciated. During the 1- and 2-cell stages, the majority (60 % and 85 %, respectively) of the analyzed proteins exhibit twofold or greater changes in their rates of synthesis. The periods of greatest change are the late 1-cell and mid 2-cell stages, during which an extensive remodelling of protein synthetic pattern occurs that is largely complete by 15 h following the first cleavage. Once this reprogramming is complete, very little change is observed during the late 2-cell and 4-cell stages. Cluster analysis of individual protein synthesis patterns reveals a limited number of coordinately regulated protein sets that are responsible for most of the changes observed during the and 2-cell stages. During the 2-cell stage, one third of the proteins increase by an average of fivefold, another third decrease by an average of sevenfold, and 10% undergo transient changes in rates of synthesis. These patterns reflect the switch from zygotic to maternal mRNA utilization following transcriptional activation. Significantly, a set of proteins exhibiting relatively constant rates of synthesis is not observed during the 2-cell stage, indicating that the rate of synthesis of almost every detectable protein changes significantly during this period. Overall, our data indicate that the transition from maternal to embryonic control of development results in an abrupt and extensive reprogramming of the early embryo with respect to the pattern of proteins synthesized.
Segmentation gene expression in the housefly Musca domestica
Authors: Sommer Ralf , Tautz Diethard 
Published: April 2021

ABSTRACT
Drosophila and Musca both belong to the group of higher dipteran flies and show morphologically a very similar early development. However, these two species are evolutionary separated by at least 100 million years. This presents the opportunity for a comparative analysis of segmentation gene expression across a large evolutionary distance in a very similar embryonic background. We have analysed in detail the early expression of the maternal gene bicoid, the gap genes hunchback, Krüppel, knirps and tailless, the pair-rule gene hairy, the segmentpolarity gene engrailed and the homoeotic gene Ultrabithorax. We show that the primary expression domains of these genes are conserved, while some secondary expression aspects have diverged. Most notable is the finding of hunchback expression in 11 –13 stripes shortly before gastrulation, as well as a delayed expression of terminal domains of various genes. We conclude that the early developmental gene hierarchy, as it has been defined in Drosophila, is evolutionary conserved in Musca domestica.
Drosophila PS integrins recognize vertebrate vitronectin and function as cell-substratum adhesion receptors in vitro
Authors: Hirano Shinji , Ui Kumiko , Miyake Tadashi , Uemura Tadashi , Takeichi Masatoshi 
Published: April 2021

ABSTRACT
Using the Drosophila cell line MLDmBG-1, a monoclonal antibody aBG-1 that can inhibit not only cell clumping but also cell spreading was generated. This antibody immunoprecipitates a complex of molecules consisting of a major 120×103Mr and other components. To characterize the 120×103Mr component, we purified it, generated antibodies to it, and cloned its cDNA. Sequencing of this cDNA suggests that the 120×103Mr molecule is identical to PSβ, a β chain of Drosophila integrins. The other components immunoprecipitated included two a chains of Drosophila integrins, PSlα and PS2α, as revealed using specific antibodies to these molecules. These suggest that aBG-1 recognizes the PSβ associated with PSlα or PS2α. However, immunostaining of embryos and larvae with aBG-1 showed that the staining pattern is similar to that for PS2α but not for PSβ, suggesting that the antibody preferentially recognizes the PSβ associated with particular a chains in situ. We then attempted to characterize the ligands for these integrin complexes, using culture dishes coated with various vertebrate matrix proteins. These cells spread very well on dishes coated with vitronectin and, to a lesser extent, on those with fibronectin. This spreading was partially inhibited by aBG-1, but not by other control antibodies or RGD peptides. The cell attachment to these substrata was not affected by the antibody. The cells also can attach to dishes coated with laminin but without spreading, and this attachment was not inhibited by aBG-1. Furthermore, they do not attach to dishes coated with collagen type I, type IV, and fibrinogen. These results indicate that Drosophila PS integrins can recognize vertebrate vitronectin, and also fibronectin with a weaker affinity, at sites other than RGD sequences, and thus can function in cell-substratum adhesion.
Regeneration of the root pole in surgically transected carrot embryos occurs by position-dependent, proximodistal replacement of missing tissues
Authors: Schiavone F. M. , Racusen R. H. 
Published: April 2021

ABSTRACT
Torpedo-stage carrot embryos were surgically transected at various locations along the shoot-root axis and explants of the cotyledon-bearing shoot pole were sectioned and examined in order to provide a more detailed description of root pole regeneration. When excisions occurred at the sites of the future hypocotyl, the future radicle or the future root apical meristem, the regenerating axial tissues exhibited patterns of cellular organization that were nearly identical to those seen in unsevered controls. To accomplish this restoration, new cells, of the type normally found at each cutting site, were produced behind a regeneration dome that formed over the original surgical site. The regeneration dome was displaced by division and expansion-driven extension of the longitudinal axis, and cells in the renewed region quickly acquired individual anatomical traits and collective tissue morphologies that corresponded to those of cells in the analogous locations in intact embryos. Although no clear mechanism is implied, the results of these experiments suggest that interactions between cells near the surgical margin permit them to retain their-sense of location within the original structure, and apprise them of the removal of their basipetally positioned neighbors. With varying-length remnants of the shoot serving as the only vestige of the original size and shape of the embryo, cells close to the site of excision were apparently reconfigured to commence ordered divisions that ultimately reconstituted the embryonic axis.
Response to fibronectin of mouse primordial germ cells before, during and after migration
Authors: Ffrench-Constant Charles , Hollingsworth Andrew , Heasman Janet , Wylie Christopher C. 
Published: April 2021

ABSTRACT
The adhesive extracellular matrix glycoprotein fibronectin is thought to play a central role in cell migration during embryogenesis. In order to define this role, we have examined the response to fibronectin in cell culture of mouse primordial germ cells (PGCs) before, during and after their migration from the hindgut into their target tissue, the genital ridges. Using an explant culture system, we show that PGCs will emigrate from tissue fragments containing hindgut, and that fibronectin stimulates this migration. Adhesion assays show that the start of PGC migration is associated with a fall in adhesion to fibronectin. Double-labelling studies using in situ hybridization and histochemistry demonstrate that migrating PGCs do not contain detectable fibronectin mRNA, suggesting that they do not synthesize and secrete the fibronectin within their migratory substratum. Taken together, these findings are consistent with an important role for fibronectin in stimulating PGC migration. In addition, however, they suggest that the interaction between PGCs and fibronectin may be important in timing the start of migration, with the fall in adhesion allowing the PGCs to commence their migration towards the genital ridges.
Altered expression of the chicken homeobox-containing genes GHox-7 and GHox-8 in the limb buds of limbless mutant chick embryos
Authors: Coelho Caroline N. D. , Krabbenhoft Karen M. , Upholt William B. , Fallon John F. , Kosher Robert A. 
Published: April 2021

ABSTRACT
It has been suggested that the reciprocal expression of the chicken homeobox-containing genes GHox-8 and GHox-7 by the apical ectodermal ridge and subjacent limb mesoderm might be involved in regulating the proximodistal outgrowth of the developing chick limb bud. In the present study the expression of GHox-7 and GHox-8 has been examined by in situ and dot blot hybridization in the developing limb buds of limbless mutant chick embryos. The limb buds of homozygous mutant limbless embryos form at the proper time in development (stage 17/18), but never develop an apical ectodermal ridge, fail to undergo normal elongation, and eventually degenerate. At stage 18, which is shortly following the formation of the limb bud, the expression of GHox-7 is considerably reduced (about 3-fold lower) in the mesoderm of limbless mutant limb buds compared to normal limb bud mesoderm. By stages 20 and 21, as the limb buds of limbless embryos cease outgrowth, GHox-7 expression in limbless mesoderm declines to very low levels, whereas GHox-7 expression increases in the mesoderm of normal limb buds which are undergoing outgrowth. In contrast to GHox-7, expression of GHox-8 in limbless mesoderm at stage 18 is quantitatively similar to its expression in normal limb bud mesoderm, and in limbless and normal mesoderm GHox-8 expression is highly localized in the anterior mesoderm of the limb bud. In normal limb buds, GHox-8 is also expressed in high amounts by the apical ectodermal ridge. However, expression of GHox-8 is severely impaired in the ectoderm of limbless mutant limb buds, which lack an apical ectodermal ridge. The severely impaired expression of GHox-7 in the mesoderm of limbless limb buds suggests that the normal expression of GHox-7 by limb mesoderm during limb bud outgrowth may be regulated by the apical ectodermal ridge, and further suggests the possibility that expression of GHox-7 by subridge mesenchymal cells may be required for normal limb outgrowth to occur. Furthermore, the severely impaired expression of GHox-8 by limbless ectoderm suggests GHox-8 may indeed be involved in ridge function. These observations also raise the interesting possibility that normal GHox-8 expression by the apical ectodermal ridge may be required for normal expression of GHox-7 by the subridge mesenchymal cells.
Genetic and cytological control of the asymmetric divisions that pattern the Volvox embryo
Authors: Kirk David L. , Kaufman Melissa R. , Keeling Richard M. , Stamer Kandace A. 
Published: April 2021

Abstract
The highly regular pattern in which approximately 2000 small somatic cells and 16 large reproductive cells (or ‘gonidia’) are arranged in a typical asexual adult of Volvox carteri can be traced back to a stereotyped program of embryonic cleavage divisions. After five symmetrical divisions have produced 32 cells of equal size, the anterior 16 cells cleave asymmetrically, to produce one small somatic cell initial and one larger gonidial initial each. The gonidial initials then cease dividing before the somatic cell initials do. The significance of the visibly asymmetric divisions is underscored by genetic and experimental evidence that differences in size - rather than differences in cytoplasmic quality - are causally important in activating the programs that cause small cells to become mortal somatic cells and large cells to differentiate as reproductive cells. A number of loci, including at least five mul (‘multiple gonidia’) loci, appear to be responsible for determining where and when asymmetric divisions will occur, since mutations at these loci result in modified temporal and/or spatial patterns of asymmetric division in one or more portions of the life cycle. But the capacity to divide asymmetrically at all appears to require a function encoded by the gls (gonidialess) locus, since gls mutants fail to execute any asymmetric divisions. Second-site suppressors of gls that have been identified may encode other functions required for asymmetric division. Cytological and immunocytochemical studies of dividing embryos are being undertaken in an attempt to elucidate the mechanisms by which cell-division planes are established - and shifted - under the influence of such pattern-specifying genes. Studies to date clearly indicate a central role for the basal body apparatus, and particularly its microtubular rootlets, in establishing the orientation of both the mitotic spindle and the cleavage furrow; but it remains to be determined how behavior of the division apparatus becomes modified during asymmetric division.