bluuebunny/crossref_metadata_2025_split huggingface dataset:
Retinoic acid stage-dependently alters the migration pattern and identity of hindbrain neural crest cells
Authors: Lee You Mie , Osumi-Yamashita Noriko , Ninomiya Youichirou , Moon Chang Kiu , Eriksson Ulf , Eto Kazuhiro 
Published: April 2021

ABSTRACT
This study investigates the migration patterns of cranial neural crest cells in retinoic acid (RA)-treated rat embryos using DiI labeling. Wistar-Imamichi rat embryos were treated at the early (9.0 days post coitum, d.p.c.) and late (9.5 d.p.c.) neural plate stages with all-trans RA (2×10-7 M) for 6 hours and further cultured in an RA-free medium. RA exposure stage dependently induced two typical cran-iofacial abnormalities; that is, at 9.0 d.p.c. it reduced the size and shape of the first branchial arch to those of the second arch, whereas, in contrast, at 9.5 d.p.c. it induced fusion of the first and second branchial arches. Early-stage treatment induced an ectopic migration of the anterior hindbrain (rhombomeres (r) 1 and 2) crest cells; they ectopically distributed in the second branchial arch and acousticofacial ganglion, as well as in their original desti-nation, i.e., the first arch and trigeminal ganglion. In contrast, late-stage treatment did not disturb the segmental migration pattern of hindbrain crest cells even though it induced the fused branchial arch (FBA); labeled crest cells from the anterior hindbrain populated the anterior half of the FBA and those from the preotic hindbrain (r3 and r4) occupied its posterior half. In control embryos, cellular retinoic acid binding protein I (CRABP I) was strongly expressed in the second branchial arch, r4 and r6, while weakly in the first arch and r1-3. CRABP I was up-regulated by the early-stage treatment in the first branchial arch and related rhombomeres, while its expression was not correspondingly changed by the late-stage treatment. Moreover, whole-mount neurofilament staining showed that, in early-RA-treated embryos, the typical structure of the trigeminal ganglion vanished, whereas the late-stage-treated embryos showed the feature of the trigeminal ganglion to be conserved, although it fused with the acousticofacial ganglion. Thus, from the standpoints of morphology, cell lineages and molecular markers, it seems likely that RA alters the regional identity of the hindbrain crest cells, which may correspond to the transformation of the hindbrain identity in RA-treated mouse embryos (Marshall et al., Nature 360, 737-741, 1992).
The mouse homolog of the orphan nuclear receptor tailless is expressed in the developing forebrain
Authors: Monaghan A. Paula , Grau Evelyn , Bock Dagmar , Schütz Günther 
Published: April 2021

ABSTRACT
The Drosophila tailless gene is a member of the orphan nuclear receptor subfamily. In Drosophila, the tailless gene is required for pattern formation in embryonic poles. During development, tailless is activated in the termini of the embryo in response to the torso receptor tyrosine kinase signal transduction cascade. Recessive mutations of tailless result in abnormalities in anterior portions of the head and in all structures posterior to the eighth abdominal segment. Localised expression of tailless is required in combination with a second terminal gene, huckebein, to control the expression of downstream genes.
We have isolated a mouse homolog of the Drosophila tailless gene, which shows considerable homology in the DNA-binding domain suggesting that the respective proteins bind similar recognition sequences. Although the ligand-binding domain shows features in common with the tailless ligand domain, it also shares conserved amino acid stretches with other orphan nuclear receptors, the human ovalbumin upstream binding protein transcription factors (hCOUP-TF I and II). We have analysed the expression of tailless in mice, and show that it is specifically localised to the developing forebrain from day 8 p.c. and in dorsal midbrain from day 8.75 p.c. To define the anterior and posterior boundaries of expression, we compared the expression pattern of tailless to those of other forebrain markers, including distal-less (Dlx1), brain factor 1 (BF1), and the orthodenticle genes (Otx1 and Otx2). In addition to the developing forebrain, these genes show dynamic patterns of expression in two structures whose development requires inductive signals from the forebrain: the eye and the nose. These results suggest that the mouse tailless gene may be required to pattern anterior brain differentiation.
Cell dispersion patterns in different cortical regions studied with an X-inactivated transgenic marker
Authors: Tan S.-S. , Faulkner-Jones B. , Breen S. J. , Walsh M. , Bertram J. F. , Reese B. E. 
Published: April 2021

ABSTRACT
Inactivation of the X-linked lacZ transgene provides a novel and powerful way of distinguishing between clonally related cellular populations in X inactivation mosaics. This ability to distinguish between clonal populations of cells in the mature cortex permits inferences to be made about cellular dispersion patterns during cortical development. The present study addresses the extent to which radial and tangential dispersion patterns contribute to different regions of the cerebral cortex by quantifying the extent of cellular mixing between clonally distinct cells in separate domains of the medial, dorsolateral and lateral cortices. We show that stripes running perpendicular to the cortical layers are more likely to be seen in the medial and dorsolateral regions, and that the appearance of a stripe is attributed to about two-thirds of the cells being of the same colour. Both neurons and glia appeared to exhibit the same ratio of cell mixing. In the lateral regions of the cortex, stripes were not apparent, and cell mixing was roughly equal. In the barrel-field region of the somatosensory cortex we looked for a correspondence between cytoarchitectural features and clonal borders but found no correlation. These results demonstrate, first, that although there is widespread radial dispersion, no cortical region is composed of radially arrayed stripes of cells in which all members of a stripe are derived from a single progenitor. Second, they demonstrate that, within regions containing a sizeable fraction of cells that do migrate radially, the boundaries of individual stripes do not always coincide with single anatomical units of cortical specialization, such as individual barrels.
Nuclei from fertilized mouse embryos have calcium-releasing activity
Authors: Kono Tomohiro , Carroll John , Swann Karl , Whittingham David G. 
Published: April 2021

ABSTRACT
During mammalian fertilization, the sperm triggers a series of intracellular Ca2+ oscillations which initiate oocyte activation and the formation of pronuclei. Oocyte activation can be induced artificially by a variety of chemical and physical stimuli which elevate intracellular calcium. We show that the transfer of nuclei from 1and 2-cell-stage fertilized mouse embryos to unfertilized oocytes stimulates the completion of meiosis and the formation of pronuclei. Nuclei from embryos that had developed to the 4-cell stage did not stimulate meiotic resumption. The ability to cause oocyte activation was specific to nuclei transferred from fertilized embryos as nuclei from parthenogenetic embryos or cytoplasts from fertilized or parthenogenetic embryos did not induce activation. Nucleus-induced oocyte activation was associated with the generation of intracellular Ca2+ transients, which were seen after nuclear envelope breakdown of the transferred nuclei. Treatment of the oocyte with the intracellular Ca2+ chelator, BAPTA, prior to nuclear transfer inhibited intracellular Ca2+ transients and oocyte activation. The specific Ca2+-releasing activity of the nucleus was not caused by sperm-induced protein synthesis since similar activity was present in nuclei originating from embryos exposed to cycloheximide throughout fertilization. The specific ability of nuclei from fertilized embryos to stimulate Ca2+ transients and oocyte activation was also found in nuclei from embryos parthenogenetically activated by the injection of a partially purified cytosolic sperm factor. The results suggest that the fertilizing sperm introduces Ca2+-releasing activity which becomes associated with the nucleus of early mammalian embryos.
Rhombomeric origin and rostrocaudal reassortment of neural crest cells revealed by intravital microscopy
Authors: Birgbauer Eric , Sechrist John , Bronner-Fraser Marianne , Fraser Scott 
Published: April 2021

ABSTRACT
Neural crest cell migration in the hindbrain is segmental, with prominent streams of migrating cells adjacent to rhombomeres (r) r2, r4 and r6, but not r3 or r5. This migratory pattern cannot be explained by the failure of r3 and r5 to produce neural crest, since focal injections of the lipophilic dye, DiI, into the neural folds clearly demonstrate that all rhombomeres produce neural crest cells. Here, we examine the dynamics of hindbrain neural crest cell emigration and movement by iontophoretically injecting DiI into small numbers of cells. The intensely labeled cells and their progeny were repeatedly imaged using low-light-level epifluorescence microscopy, permitting their movement to be followed in living embryos over time. These intravital images definitively show that neural crest cells move both rostrally and caudally from r3 and r5 to emerge as a part of the streams adjacent to r2, r4, and/or r6. Within the first few hours, cells labeled in r3 move within and/or along the dorsal neural tube surface, either rostrally toward the r2/3 border or caudally toward the r3/4 border. The labeled cells exit the surface of the neural tube near these borders and migrate toward the first or second branchial arches several hours after initial labeling. Focal DiI injections into r5 resulted in neural crest cell contributions to both the second and third branchial arches, again via rostrocaudal movements of the cells before migration into the periphery. These results demonstrate conclusively that all rhombomeres give rise to neural crest cells, and that rostrocaudal rearrangement of the cells contributes to the segmental migration of neural crest cells adjacent to r2, r4, and r6. Furthermore, it appears that there are consistent exit points of neural crest cell emigration; for example, cells arising from r3 emigrate almost exclusively from the rostral or caudal borders of that rhombomere.
The role of Pax-6 in eye and nasal development
Authors: Grindley Justin C. , Davidson Duncan R. , Hill Robert E. 
Published: April 2021

ABSTRACT
Small eye (Sey) mice homozygous for mutations in the Pax-6 gene have no lenses and no nasal cavities. We have examined the ontogeny of eye and nasal defects in Sey/Sey embryos and have related the defects seen to the pattern of Pax-6 mRNA expression in the mouse during normal eye and nasal development.
There are two principal components of the early eye, the neural ectoderm of the optic vesicle, which forms the retina, and the overlying surface ectoderm, which forms the lens and cornea. By studying these interacting tissues in normal and Sey/Sey embryos, we have identified processes for which Pax-6 is important and can thus suggest possible roles for the Pax-6 gene.
Pax-6 is essential for the formation of lens placodes from surface ectoderm. In normal development, early Pax-6 mRNA expression in a broad domain of surface ectoderm is downregulated, but expression is specifically maintained in the developing lens placode. Moreover, other Pax-6expressing tissues are frequently those that have can transdifferentiate into lens. Thus, phenotype and expression together suggest a role for Pax-6 in lens determination.
At least some functions of Pax-6 can be separated from the influence of other tissues. Early Sey/Sey optic vesicles are abnormally broad and fail to constrict proximally. These defects occur prior to the time of lens placode formation and probably reflect a requirement for Pax-6 in neural ectoderm. In surface ectoderm domains, where Pax6 expression is known to be independent of the presence of an optic vesicle, Pax-6 function is required for the maintenance of its own transcription.
The mutual dependency of lens and optic vesicle development can also be studied using the Small eye mutation. Using region-specific markers we find that, in the morphologically abnormal Sey/Sey optic vesicles, aspects of normal proximo-distal specification nevertheless persist, despite the complete absence of lens.
Like the lens, the nasal cavities develop from ectodermal placodes that normally express Pax-6 mRNA, fail to form in Sey/Sey mice and show Pax-6-dependent Pax-6 mRNA regulation. Analysis of patterns of programmed cell death and absence of nasal region expression from an Msx-1 transgene in Sey/Sey embryos suggest a requirement for Pax-6 in the transition from presumptive nasal ectoderm to placode, and that Msx-1, or genes regulating it, are possible targets for Pax-6.
Tissue non-specific alkaline phosphatase is expressed in both embryonic and extraembryonic lineages during mouse embryogenesis but is not required for migration of primordial germ cells
Authors: MacGregor Grant R. , Zambrowicz Brian P. , Soriano Philippe 
Published: April 2021

ABSTRACT
Mouse primordial germ cells express tissue non-specific alkaline phosphatase (TNAP) during development, but the widespread expression of another alkaline phosphatase gene in the early embryo limits the potential use of this marker to trace germ cells. To attempt to identify germ cells at all stages during embryonic development and to understand the role of TNAP in germ cell ontogeny, mice carrying a βgeo (lacZ/neor) disrupted allele of the TNAP gene were generated by homologous recombination in embryonic stem cells. Using β-galactosidase activity, the embryonic pattern of TNAP expression was examined from the blastocyst stage to embryonic day 14. Results indicate that primordial germ cell progenitors do not express TNAP prior to gastrulation although at earlier times TNAP expression is found in an extraembryonic lineage destined to form the chorion. In homozygous mutants, primordial germ cells appear unaffected indicating that TNAP is not essential for their development or migration.
Autonomous and non-autonomous differentiation of ectoderm in different sea urchin species
Authors: Wikramanayake Athula H. , Brandhorst Bruce P. , Klein William H. 
Published: April 2021

ABSTRACT
During early embryogenesis, the highly regulative sea urchin embryo relies extensively on cell-cell interactions for cellular specification. Here, the role of cellular interactions in the temporal and spatial expression of markers for oral and aboral ectoderm in Strongylocentrotus purpuratus and Lytechinus pictus was investigated. When pairs of mesomeres or animal caps, which are fated to give rise to ectoderm, were isolated and cultured they developed into ciliated embryoids that were morphologically polarized. In animal explants from S. purpuratus, the aboral ectodermspecific Spec1 gene was activated at the same time as in control embryos and at relatively high levels. The Spec1 protein was restricted to the squamous epithelial cells in the embryoids suggesting that an oral-aboral axis formed and aboral ectoderm differentiation occurred correctly. However, the Ecto V protein, a marker for oral ectoderm differentiation, was detected throughout the embryoid and no stomodeum or ciliary band formed. These results indicated that animal explants from S. purpuratus were autonomous in their ability to form an oral-aboral axis and to differentiate aboral ectoderm, but other aspects of ectoderm differentiation require interaction with vegetal blastomeres. In contrast to S. purpuratus, aboral ectodermspecific genes were not expressed in animal explants from L. pictus even though the resulting embryoids were morphologically very similar to those of S. purpuratus. Recombination of the explants with vegetal blastomeres or exposure to the vegetalizing agent LiCl restored activity of aboral ectoderm-specific genes, suggesting the requirement of a vegetal induction for differentiation of aboral ectoderm cells. These results demonstrate that differences exist in aboral ectoderm differentiation between S. purpuratus and L. pictus and suggest that the formation of a cell type may occur by alternative mechanisms in two related species.
Arabidopsis gynoecium structure in the wild type and in ettin mutants
Authors: Sessions R. Allen , Zambryski Patricia C. 
Published: April 2021

ABSTRACT
The gynoecium is the female reproductive structure of flowering plants. Here we present a description of the Arabidopsis thaliana gynoecium at anthesis. The cylindrical organ can be broken down into three longitudinal regions arranged in an apical-basal order: stigma, style, and ovary. Each region can be distinguished histologically and morphologically. The transmitting (pollination) tract is axially positioned along the center of the gynoecium and spans stigma, style and ovary. Histochemistry, scanning electron microscopy and a style-specific reporter gene are used to compare the wild-type pattern of gynoecium cell types and regions, with patterns formed in gynoecia of individuals homozygous for a series of allelic mutations at the ETTIN locus. ettin gynoecia show morphological and histological alterations that appear to result from the merging of apical and basal regions and the development of abaxial into adaxial tissues. These developmental abnormalities result in a reduction of the ovary region, an expansion of the stylar and stigmatic regions, and the abaxial (outward) proliferation of transmitting tract tissue. The alterations in the mutants can be interpreted as resulting from misspecifications of position along the longitudinal and transverse axes during gynoecium development. The results suggest that early patterning events underlie wild-type gynoecium development, and that ETT functions during this early programming.
Notch1 is required for the coordinate segmentation of somites
Authors: Conlon Ronald A. , Reaume Andrew G. , Rossant Janet 
Published: April 2021

ABSTRACT
Members of the Notch family of transmembrane receptors mediate a number of developmental decisions in invertebrates. In order to study Notch function in a vertebrate organism, we have mutated the Notch1 gene of the mouse. Notch1 gene function is required for embryonic survival in the second half of gestation. In the first half of gestation, we have found no effect of the mutation on the normal programs of neurogenesis, myogenesis or apoptosis. We conclude that Notch1 function is not essential for these processes, at least in early postimplantation development. However, we have found that somitogenesis is delayed and disorganized in Notch1 mutant embryos. We propose that Notch1 normally coordinates the process of somitogenesis, and we provide a model of how this might occur.
Dorsal wing, a locus that affects dorsoventral wing patterning in Drosophila
Authors: Tiong Stanley Y. K. , Nash David , Bender Welcome 
Published: April 2021

ABSTRACT
The wing imaginal disc is subdivided into a dorsal and a ventral compartments. A new dominant homeotic mutation, Dorsal wing1 (Dlw1), transforms ventral into dorsal compartment in heterozygotes. This phenotype is similar to one of the dominant phenotypes of Polycomb (Pc) mutants. In Pc Dlw+/Pc+Dlw1 double mutants, the trans formation is greatly enhanced. The recessive phenotype of Dlw1 is the opposite to the dominant phenotype. Dlw1/Dlw1 somatic clones induced at any larval stage differentiate only ventral pattern on both wing surfaces. This effect is one of the somatic clone phenotypes of trithorax (trx) lethals. A similar dorsal-to-ventral transformation is observed in Pc Dlw/Dlw clones. Dlw1/Dlw1 clones have no effect elsewhere, except in the dorsal notum, which may differentiate extra macrochaetes. We propose that: (1) Dlw+ is required for the specification of dorsal compartment; (2) some genes of the Polycomb group act as negative regulators of Dlw+, while some genes of the trithorax group act as positive regulators.
Inserting the Ftz homeodomain into Engrailed creates a dominant transcriptional repressor that specifically turns off Ftz target genes in vivo
Authors: John Aleyamma , Smith Sheryl T. , Jaynes James B. 
Published: April 2021

ABSTRACT
The Engrailed homeodomain protein is an ‘active’ or dominant transcriptional repressor in cultured cells. In contrast, the Fushi Tarazu homeodomain protein is an activator, both in cultured cells and in Drosophila embryos, where it activates several known target genes, including its own gene. This auto-activation has been shown to depend on targeting to a fushi tarazu enhancer by the Fushi Tarazu homeodomain. We combined Fushi Tarazu targeting and Engrailed active repression in a chimeric regulator, EFE. When EFE is ubiquitously expressed, it overrides endogenous Fushi Tarazu and causes a fushi tarazu mutant phenotype. Normal Fushi Tarazu target genes are affected as they are in fushi tarazu mutants. One such target gene is repressed by EFE even where Fushi Tarazu is not expressed, suggesting that the repression is active. This is confirmed by showing that the in vivo activity of EFE depends on a domain that is required for active repression in culture. A derivative that lacks this domain, while it cannot repress the endogenous fushi tarazu gene, can still reduce the activity of the fushi tarazu autoregulatory enhancer, suggesting that it competes with endogenous Fushi Tarazu for binding sites in vivo. However, this passive repression is much less effective than active repression.
Control of epithelial morphogenesis by cell signaling and integrin molecules in the Drosophila foregut
Authors: Pankratz Michael J. , Hoch Michael 
Published: April 2021

ABSTRACT
Coordinated cell movements are critical for tissue and organ morphogenesis in animal development. We show that the Drosophila genes hedgehog and wingless, which encode signaling molecules, and the gene myospheroid, which encodes a β subunit of the integrins, are required for epithelial morphogenesis during proventriculus development. In contrast, this morphogenetic process is suppressed by the decapentaplegic gene, which encodes a member of the TGFβ family of growth factors. These results identify a novel cell signaling center in the foregut that directs the formation of a multiply folded organ from a simple epithelial tube.