pinecone/core-2020-05-10-deduplication huggingface dataset:
Retarded Postimplantation Development of X0 Mouse Embryos: Impact of the Parental Origin of the Monosomic X Chromosome

AbstractAbout 12–17% of the embryos obtained by mating mice carrying the In(X)1H orPafmutations are of the 39,X (X0) genotype. Depending on the mutant mice used for mating, the monosomic X chromosome can be inherited from the paternal (XP) or the maternal (XM) parent. The XP0 embryos display developmental retardation at gastrulation and early organogenesis. XP0 embryos also display poor development of the ectoplacental cone, which is significantly smaller in size and contains fewer trophoblasts than XX siblings. In contrast, XM0 embryos develop normally and are indistinguishable from XX littermates. In both types of X0 embryos, an X-linkedlacZtransgene is expressed in nearly all cells in both the embryonic and the extraembryonic tissues, suggesting that X inactivation does not occur when only one X is present. Of particular significance is the maintenance of an active XPchromosome in the extraembryonic tissues where normally the paternal X chromosome is preferentially inactivated in XX embryos. The differential impact of the inheritance of X chromosomes from different parents on the development of the X0 embryos raises the possibility that the XPis less capable than the XMin providing the appropriate dosage of X-linked activity that is necessary to support normal development of the embryo and the ectoplacental cone. Alternatively, the development of the XP0 embryo may be compromised by the lack of activity of one or several X-linked genes which are expressed only from the maternal X chromosome. Without the activity of these genes, embryonic development may be curtailed even though all other loci on the XPchromosome are actively transcribed
Early Migrating Neural Crest Cells Can Form Ventral Neural Tube Derivatives When Challenged by Transplantation

AbstractOnce neural crest cells undergo an epithelial–mesenchymal transition to leave the neural tube, it has been classically assumed that they are fated to differentiate within the neural crest lineage. To test this idea, we challenged the developmental potential of recently emigrated neural crest cells by transplanting them into the ventral portion of the neural tube at the open neural plate stage. Newly migrating neural crest cells were isolated in tissue culture, labeled with the lipophilic dye DiI, and microinjected into the ventral portion of the neural plate. After 2 days, some neural crest cells became incorporated into the neuroepithelium in positions characteristic of floor plate cells and motor neurons. Some of the labeled cells within the ventral neural tube expressed FP-1, characteristic of floor plate cells. A few labeled cells were found in positions characteristic of motor neurons and expressed islet-1. In contrast, neural crest cells transplanted onto neural crest pathways expressed the HNK-1 epitope, but no ventral neural tube markers. Injection of neural crest cells into the mesenchyme adjacent to the notochord or culturing them in the presence of Sonic hedgehog failed to elicit FP-1 expression. These results suggest that migrating neural crest cells are flexible in their fate and retain the ability to form neural tube derivatives even after emigrating from the neural tube
The Expression Pattern of Thyroid Hormone Response Genes in Remodeling Tadpole Tissues Defines Distinct Growth and Resorption Gene Expression Programs

AbstractThyroid hormone (TH) induces dramatic skeletal and tissue remodeling of the anuran head and body at metamorphosis. The expression pattern of TH up-regulated genes has been correlated with tissues that either grow or resorb at metamorphosis. Whereas the expression of the thyroid hormone receptors inXenopus laevistadpoles is ubiquitous, the locations where many of the TH up-regulated genes are activated fall into distinct classes. Genes in the early response class are expressed predominantly in cartilage and brain regions undergoing cell proliferation and at a higher level in the remodeling and growing body than in the resorbing tail. In contrast, expression of genes in the delayed response class is highest in resorbing tissues and higher in the tail than in the body within the subepidermal fibroblast layer, further indicating that this single cell layer is involved in tissue resorption. The expression boundary of delayed response class genes in the subepidermal fibroblasts in the body correlates with epidermal lamella invasion and subsequent adult skin differentiation. Differences in the expression patterns of stromelysin-3 and the delayed response proteinases in the head delineate separate programs of tissue resorption, one for the loss of epithelial structures, and one for the loss of cartilages. Expression of the type III deiodinase is up-regulated in growing tissues nearing completion of their metamorphic changes, suggesting a role for the deiodinase in modulating the influence of TH on these tissues
Notochord Regulates Cardiac Lineage in Zebrafish Embryos

AbstractWe focus here upon regulation by the notochord of myocardial cell fate in zebrafish. Myocardial precursors, defined by lineage tracing in the living embryo, are in the lateral plate mesoderm adjacent to the notochord-prechordal plate junction. Interestingly, the anterior end of the notochord corresponds to the posterior extent of the heart progenitor field, defined by this lineage analysis. This suggested that the notochord might suppress, or the prechordal plate might enhance, the cardiogenic fate.Nkx2.5expression is, in the zebrafish embryo, closely correlated with the position of myocardial precursors, which reside adjacent to the notochord–prechordal plate junction. This expression, however, is extinguished in the region posterior to this junction, a region normally not contributing cells to the heart. Laser ablation of the notochord tip between the 4-somite and 12-somite stage causes posterior expansion of theNkx2.5-expressing region. Thentlmutation of the notochord is associated with posterior extension ofNkx2.5expression. Lineage tracking, by laser activation of caged fluoresceinated dextran, confirms that, normally, lateral plate cells next to the notochord do not contribute progeny to the heart. After anterior notochord ablation, these cells are redirected to a heart cell fate. These data suggest that the anterior notochord delimits the posterior extent of the heart field by suppressing the heart cell fate
Mannose-Specific Recognition Mediates Two Aspects of Synaptic Growth of Leech Sensory Afferents: Collateral Branching and Proliferation of Synaptic Vesicle Clusters

AbstractThe developmental role of carbohydrate markers in the genesis of neuronal networks was studied using leech sensory afferents as a model. Leech sensory afferents express a mannose-containing epitope on their cell surface that is recognized by monoclonal antibody Lan3-2. Previously, the elaboration of sensory arbors in the synaptic neuropil of CNS ganglia was experimentally shown to depend on this mannose marker. Sensory arbors were abolished by perturbing sensory afferents in the intact nervous system with Lan3-2 Fab fragments, a glycosidase, or mannose–BSA. To understand the cytological mechanisms underlying mannose-specific recognition for synaptogenesis, we have now studied the effects of antibody perturbation at the ultrastructural level in the sensory afferent target region. A characteristic signature of a normal sensory afferent is its profuse collateral branching, which, with ongoing development, is replaced by a single widened process, the sensory trunk, which possesses numerous synaptic vesicle clusters. The inhibition of mannose-specific recognition leads to a rapid, major reorganization of different stages of sensory afferent growth. Collateral branches at the distal growing region are reduced three- to fourfold. The pruned axons grow at an accelerated rate. Developmentally older sensory trunks experience a threefold reduction in synaptic vesicle clusters. These responses suggest that depriving sensory afferents of mannose-specific recognition aborts their synaptogenesis and causes them to resume behavior typical of tracking through axonal tracts. The current findings also suggest that the mannose marker, by promoting both collateral branching andthe proliferation of synaptic vesicle clusters, plays a critical role in two stages of sensory afferent synaptogenesis
Normal Reproductive and Macrophage Function inPemHomeobox Gene-Deficient Mice

AbstractInteraction between germ cells and the supporting somatic cells guides many of the differentiative processes of gametogenesis. The expression pattern of thePemhomeobox gene suggests that it may mediate specific inductive events in murine reproductive tissues. During gestation,Pemis expressed in migrating and early postmigratory primordial germ cells, as well as in all embryo-derived extraembryonic membranes.Pemexpression ceases in the germline after Embryonic Day 14 in both sexes and then reappears postnatally in the supporting cells of the gonad. In mature mice,Pemis produced by testicular Sertoli cells during stages VI–VIII of spermatogenesis and transiently by ovarian granulosa cells lining periovulatory follicles. Despite this tightly regulated reproductive expression pattern, mice with a targeted mutation inPemhave normal fecundity, with no detectable alteration in extraembryonic testicular or ovarian development or function. We also show thatPemis expressed throughout embryonic and adult development in a subset of a tissue-specific class of macrophages, Kupffer cells, as well as in a localized fraction of cells in macrophage cell lines. Although the number of Pem-positive Kupffer cells increases in mice treated with lipopolysaccharide, loss of Pem does not detectably interfere with the cells' ability to induce iNOS expression, demonstrating this Kupffer cell function does not requirePem.No differences were observed between Pem-knockout mice in 129, C57BL6/J, or mixed genetic backgrounds. Together, these data show thatPemis dispensable for embryonic and postnatal development, gonadal function, and Kupffer cell activation, perhaps due to compensatory expression of a similar homeobox gene
Disruption of Primary Mesenchyme Cell Patterning by Misregulated Ectodermal Expression ofSpMsxin Sea Urchin Embryos

AbstractThe patterning of the mesoderm of the sea urchin embryo is a classical paradigm of epithelial mesenchymal interactions in organogenesis, yet little is known of its molecular basis. Here we address the role of the homeobox gene,SpMsx,a member of the highly conservedMsxgene family, in this process.Msxgenes have been shown to function in the dorsoventral patterning of the central nervous system inDrosophilaand in a variety epithelial–mesenchymal interactions in vertebrates. We showed previously that theSpMsxgene is expressed during embryogenesis in a complex and dynamic pattern consistent with roles in the development of subpopulations of endoderm, mesoderm, and oral ectoderm. To perturb this pattern of expression and thus probe the function ofSpMsx,we injectedSpMsxmRNA into single-cell zygotes and monitored development morphologically and with a series of territory-specific molecular markers. RT-PCR analysis revealed that injectedSpMsxtranscripts persisted at least until the gastrula stage in amounts comparable to endogenous levels. Injected embryos exhibited deficiencies in the organization of primary and secondary mesenchyme cells within the blastocoelic cavity, as well as abnormalities in spicule number and shape. Defects in the endoderm were also common, including reduced or absent archenterons. Micromere transplantation experiments revealed that the defects in skeletogenic mesenchyme patterning were non-cell autonomous, consistent with findings that cell–cell interactions between ectoderm and the progenitors of the skeletogenic mesenchyme, the primary mesenchyme cells (PMCs), are important both for PMC guidance and spicule morphogenesis. Our data, taken together with observations in other organisms on the role ofMsxgenes in embryonic signaling processes, particularly involving the BMP pathway, suggest thatSpMsxmay be a part of the mechanism by which the ectoderm influences both the arrangement of primary mesenchyme cells within the blastocoel and the shapes of the skeletal rods
MAP Kinase Inactivation Is Required Only for G2–M Phase Transition in Early Embryogenesis Cell Cycles of the StarfishesMarthasterias glacialisandAstropecten aranciacus

AbstractDownregulation of MAP kinase is a universal consequence of fertilization in the animal kingdom. Here we show that oocytes of the starfishesAstropecten aranciacusandMarthasterias glacialiscomplete meiotic maturation and form a pronucleus when treated with 1-methyladenine and then complete DNA replication and arrest at G2 if not fertilized. Release of G2 by fertilization or a variety of parthenogenetic treatments is associated with inactivation of MAP kinase. Prevention of MAP kinase inactivation by microinjection of Ste11-ΔN, a constitutively active budding yeast MAP kinase kinase kinase, arrests fertilized eggs at G2 in either the first or the second mitotic cell cycle, in a dose-dependent manner. G1 arrest is never observed. Conversely, inactivation of MAP kinase by microinjection of the MAP kinase-specific phosphatase Pyst-1 releases mature starfish oocytes from G2 arrest. The role of MAP kinase in arresting cell cycle at various stages in oocytes of different animal species is discussed
Voltage-Dependent Activation of Frog Eggs by a Sperm Surface Disintegrin Peptide

AbstractFertilin, a sperm protein of the metalloprotease/disintegrin/cysteine-rich (MDC) family, plays a critical role in sperm–egg binding in mammals. Peptides corresponding to the disintegrin domain of fertilin and antibodies against fertilin have been shown to inhibit mammalian sperm–egg binding and fusion. A protein from the same family, xMDC16, was recently cloned from frog (Xenopus laevis) testis and was found to be involved in frog sperm–egg binding. Here we report that xMDC16 is localized predominantly on the posterior surface of egg jelly-activated sperm, and peptides from the disintegrin domain of this protein activate eggs when applied near the egg surface. Egg activation was dependent on (1) specific amino acid residues (KTX); (2) the presence of divalent cations, but not external Ca2+alone; and (3) voltage across the egg plasma membrane. This is the first demonstration of egg activation in vertebrates by the surface application of a peptide derived from a sperm surface protein, supporting a model for egg activation that involves a signal transducing receptor for sperm in the egg's plasma membrane
Sperm–Egg Binding in the Sea Urchin: A High Level of Intracellular ATP Stabilizes Sperm Attachment to the Egg Receptor

AbstractPrevious studies have established that a recombinant protein fragment (45A) of the egg receptor for sperm of the sea urchinStrongylocentrotus purpuratusexhibits several characteristics that are consistent with that expected of a receptor. Using a quantitative sperm binding assay with glutathioneS-transferase fused to a recombinant protein containing the C-terminal half of the 45A construct immobilized on glutathione beads, it was found that the interaction between sperm and this protein is a kinetically transient event. Sperm binding to the receptor fragment reached a maximum at 20 s after adding sperm in the presence of egg jelly to beads coated with recombinant receptor. In the next 20–120 s, approximately 50–70% of the sperm detached from the beads. Similar phenomena were observed when the kinetics of sperm binding to dejellied, glutaraldehyde-fixed eggs were studied. Because the acrosome reaction, a prelude to binding, is known to be accompanied by a decrease in the ATP level of sperm, we studied the effect of various inhibitors on both sperm detachment and the level of ATP. It was found that the detachment rate increased slightly when respiration inhibitors that blocked ATP production in mitochondria were added. In contrast, the dynein ATPase inhibitor,erythro-9-[3-hydroxynonyl]adenine, which is known to inhibit flagellum motility by blocking ATP utilization, stabilized the binding of sperm to the receptor and allowed maintenance of a high internal ATP level. Immotile, tailless sperm that physically lacked dynein ATPase, and therefore sustained their internal ATP levels, also exhibited stable binding provided that the sperm and beads were physically mixed. These results suggest that the internal ATP level of the sperm controls the stability of its binding to the receptor. The possible mechanism of the detachment and its significance with respect to the overall process of fertilization are discussed
The α4Subunit of Integrin Is Important for Neural Crest Cell Migration

AbstractWe identify the α4subunit of integrin as a predominant integrin expressed by neural crest cells in both avian and murine embryos. Using degenerate primers, we obtained a PCR fragment of the chick integrin α4subunit that was subsequently used to clone the full-length subunit with a predicted amino acid sequence 60% identical to human and mouse α4subunits.In situhybridization demonstrates that chick integrin α4mRNA is expressed at high levels by migrating neural crest cells and neural crest-derived ganglia at both cranial and trunk levels. An antibody against the murine α4subunit revealed similar distribution patterns in mouse to chick. In addition to neural crest cells, the integrin α4subunit was later observed on the muscle masses of the limb, the apical ectodermal ridge, and the developing liver. To examine the functional role of the integrin α4subunit in neural crest cell migration, we used an explant preparation that allows visualization of neural crest cells in their normal environment with or without perturbing reagents. In the presence of a blocking antibody against the mouse integrin α4subunit, there was a profound abrogation of neural crest cell migration at trunk and hindbrain levels. Both the numbers of migrating neural crest cells and the total distance traversed were markedly reduced. Similarly, avian embryos injected with synthetic peptides that contain the integrin α4binding site in fibronectin displayed abnormal neural crest cell migration. Our results suggest that the integrin α4subunit is important for normal neural crest cell migration and may be one of the primary α subunits used for neural crest cell migrationin vivo.Furthermore, the integrin α4subunit represents a useful neural crest marker in the mouse
The Relationship between Rhombomeres and Vestibular Neuron Populations as Assessed in Quail–Chicken Chimeras

AbstractThe aim of this study was to evaluate the role segmentation plays in the determination of neuronal identity in the hindbrain. We focused on two specific sets of hindbrain neurons, namely, the vestibulospinal and vestibulo-ocular neurons, which comprise distinct groups that can be identified and distinguished by virtue of their axonal projection pathways. The relationship between rhombomeres and the vestibular neuron groups was assessed by a combination of quail–chicken chimeric grafting and selective retrograde axonal tracing. Individual quail hemirhombomeres were transplanted homotopically and isochronically into a chicken embryo host. Subsequently, vestibulospinal and vestibulo-ocular neurons with specific axon trajectories were labeled retrogradely with biotin-conjugated dextran-amines. The relationship between the spatial domains of the vestibular neuron groups and rhombomere-derived domains had the following features: (1) some groups were derived from single rhombomeres; (2) some groups were derived from multiple contiguous rhombomeres; (3) two groups occupied domains that could not be defined in terms of whole rhombomere lengths; (4) some groups spanning multiple rhombomeres exhibited an internal cytoarchitectonic organization that related to individual rhombomeres; and (5) some groups exhibited limited boundary violation. These results support the notion that positional information within defined domains of the neural tube provides a groundplan for the regional determination of neuronal identity and axon pathfinding, and that hindbrain segmentation contributes to this process. But they also indicate that segmentation is not the only mechanism that defines the rostrocaudal domains of neuron types. Moreover, they emphasize that the relationship between rhombomeres and neuronal determination cannot be couched simply in terms of segmental iteration or of bimeric (paired rule) specification
A Single Rostrocaudal Colonization of the Rodent Intestine by Enteric Neuron Precursors Is Revealed by the Expression of Phox2b, Ret, and p75 and by Explants Grown under the Kidney Capsule or in Organ Culture

AbstractThe colonization of the rodent gastrointestinal tract by enteric neuron precursors is controversial due to the lack of specific cellular markers at early stages. The transcription factor, Phox2b, is expressed by enteric neuron precursors (Pattynet al. Development124, 4065–4075, 1997). In this study, we have used an antiserum to Phox2b to characterize in detail the spatiotemporal expression of Phox2b in the gastrointestinal tract of adult mice and embryonic mice and rats. In adult mice, all enteric neurons (labeled with neuron-specific enolase antibodies), and a subpopulation of glial cells (labeled with GFAP antibodies), showed immunoreactivity to Phox2b. In embryonic mice, the appearance of Phox2b-immunoreactive cells was mapped during development of the gastrointestinal tract. At Embryonic Days 9.5–10 (E9.5–10), Phox2b-labeled cells were present only in the stomach, and during subsequent development, labeled cells appeared as a single rostrocaudal wave along the gastrointestinal tract; at E14 Phox2b-labeled cells were present along the entire length of the gastrointestinal tract. Ret and p75 have also been reported to label migratory-stage enteric neuron precursors. A unidirectional, rostral-to-caudal colonization of the gastrointestinal tract of embryonic mice by Ret- and p75-immunoreactive cells was also observed, and the locations of Ret- and p75-positive cells within the gut were very similar to that of Phox2b-positive cells. To verify the location of enteric neuron precursors within the gut, explants from spatiotemporally defined regions of embryonic intestine, 0.3–3 mm long, were grown in the kidney subcapsular space, or in catenary organ culture, and examined for the presence of neurons. The location and sequence of appearance of enteric neuron precursors deduced from the explants grown under the kidney capsule or in organ culture was very similar to that seen with the Phox2b, Ret, and p75 antisera. Previous studies have mapped the rostrocaudal colonization of the rat intestine by enteric neuron precursors using HNK-1 as a marker. In the current study, all HNK-1-labeled cells in the gastrointestinal tract of rat embryos showed immunoreactivity to Phox2b, but HNK-1 cells comprised only a small subpopulation of the Phox2b-labeled cells. In addition, in rats, Phox2b-labeled cells were present in advance of (more caudal to) the most caudal HNK-1-labeled cells by 600–700 μm in the hindgut at E15. We conclude that the neural crest cell population that arises from the vagal level of the neural axis and that populates the stomach, midgut, and hindgut expresses Phox2b, Ret, and p75. In contrast, the sacral-level neural crest cells that populate the hindgut either do not express, or show a delayed expression of, all of the known markers of vagal- and trunk-level neural crest cells