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Morphogenetic Events (morphogenetic + event)
Selected AbstractsMorphogenesis in the Marine Spirotrichous Ciliate Apokeronopsis crassa (Claparède & Lachmann, 1858) n. comb. (Ciliophora: Stichotrichia), with the Establishment of a New Genus, Apokeronopsis n. g., and Redefinition of the Genus ThigmokeronopsisTHE JOURNAL OF EUKARYOTIC MICROBIOLOGY, Issue 4 2007CHEN SHAO ABSTRACT. Morphogenetic events during the division of the marine spirotrichous ciliate, Apokeronopsis crassa (Claparède & Lachmann 1858) n. comb. were investigated. Compared with members of the well-known genera Thigmokeronopsis, Uroleptopsis, and Pseudokeronopsis, A. crassa has one row of buccal cirri, high number of transverse cirri, clearly separated midventral rows, lacks thigmotactic cirri and a gap in adoral zone, its undulating membranes (UMs) anlage forms one cirrus and marginal rows and dorsal kineties form apokinetally during division. All these characteristics indicate that this organism represents a new taxon at the generic level, and hence a new genus is suggested, Apokeronopsis n. g. It is defined as thus: Pseudokeronopsidae with Pseudokeronopsis -like bicorona of frontal cirri and one marginal row on each side; one row of two or more buccal cirri in ordinary position; two midventral rows distinctly separated, hence of cirri that are not in a typical zig-zag pattern; high number of transverse cirri, caudal cirri absent, and frontoterminal cirri present; thigmotactic cirri absent, many macronuclear nodules fuse into many masses as well as marginal and dorsal kineties form apokinetally during morphogenesis. At the same time, the genus ThigmokeronopsisWicklow, 1981 is redefined, and one new combination, Apokeronopsis antarctica (Petz, 1995) n. comb. is proposed. The morphogenetic events of A. crassa are characterized as follows: (1) In the proter, the adoral zone of membranelles and UMs are completely renewed by the oral primordium. The UM anlage is formed apokinetally on the dorsal wall of the buccal cavity and is hence clearly separated from the frontoventral-transverse (FVT) cirral anlagen in the proter. (2) Frontoventral-transverse cirral anlagen are generated de novo in the outermost region of the cortex to the right of the old UMs. (3) A row of buccal cirri arises from FVT cirral streak I. (4) The marginal rows and dorsal kineties originate de novo in both dividers; no caudal cirri are formed. (5) The last FVT-streak contributes two frontoterminal cirri. (6) The many macronuclear nodules fuse into many masses (about 50 segments) during division, unlike a singular or branched mass as described in other urostylids. [source] Neurulation in the cranial region , normal and abnormalJOURNAL OF ANATOMY, Issue 5 2005Andrew J. Copp Abstract Cranial neurulation is the embryonic process responsible for formation of the brain primordium. In the mouse embryo, cranial neurulation is a piecemeal process with several initiation sites and two neuropores. Variation in the pattern of cranial neurulation occurs in different mouse strains, and a simpler version of this morphogenetic scheme has been described in human embryos. Exencephaly is more common in females than in males, an unexplained phenomenon seen in both mice and humans. As the cranial neural tube closes, a critical morphogenetic event is the formation of dorsolateral bending points near the neural fold tips, which enables subsequent midline fusion of the neural folds. Many mutant and gene-targeted mouse strains develop cranial neural tube defects, and analysis of the underlying molecular defects identifies several requirements for normal dorsolateral bending. These include a functional actin cytoskeleton, emigration of the cranial neural crest, spatio-temporally regulated apoptosis, and a balance between cell proliferation and the onset of neuronal differentiation. A small number of mouse mutants exhibit craniorachischisis, a combined brain and spine neurulation defect. Recent studies show that disturbance of a single molecular signalling cascade, the planar cell polarity pathway, is implicated in mutants with this defect. [source] MMP-2 contributes to the development of the mouse ventral prostate by impacting epithelial growth and morphogenesisDEVELOPMENTAL DYNAMICS, Issue 9 2010Alexandre Bruni-Cardoso Abstract Epithelial growth, branching, and canalization are important morphogenetic events of the rodent ventral prostate (VP) that take place during the first postnatal week. In this study, we evaluated the effect of knocking out MMP-2 (MMP-2,/,), by examining developmental and structural aspects of the VP in MMP-2,/, mice. Neonate (day 6) MMP-2,/, mice showed fewer epithelial tips, a lower epithelial cell proliferation rate, and also reticulin fiber accumulation. The VP of adult MMP-2,/, mice showed lower relative weight, smaller epithelial and smooth-muscle cell volume, and a larger amount of thicker reticulin fibers. No differences in cell proliferation or apoptotic index were noted between adult MMP-2,/, and wild-type mice. MMP-9 was found in the adult MMP-2,/,, but not in the wild-type. In conclusion, MMP-2 function is essential for the epithelial morphogenesis of the mouse VP, and expression of MMP-9 is not sufficient for acquisition of the normal adult histology. Developmental Dynamics 239:2386,2392, 2010. © 2010 Wiley-Liss, Inc. [source] Morphogenesis of the node and notochord: The cellular basis for the establishment and maintenance of left,right asymmetry in the mouseDEVELOPMENTAL DYNAMICS, Issue 12 2008Jeffrey D. Lee Abstract Establishment of left,right asymmetry in the mouse embryo depends on leftward laminar fluid flow in the node, which initiates a signaling cascade that is confined to the left side of the embryo. Leftward fluid flow depends on two cellular processes: motility of the cilia that generate the flow and morphogenesis of the node, the structure where the cilia reside. Here, we provide an overview of the current understanding and unresolved questions about the regulation of ciliary motility and node structure. Analysis of mouse mutants has shown that the motile cilia must have a specific structure and length, and that they must point posteriorly to generate the necessary leftward fluid flow. However, the precise structure of the motile cilia is not clear and the mechanisms that position cilia on node cells have not been defined. The mouse node is a teardrop-shaped pit at the distal tip of the early embryo, but the morphogenetic events that create the mature node from cells derived from the primitive streak are only beginning to be characterized. Recent live imaging experiments support earlier scanning electron microscopy (SEM) studies and show that node assembly is a multi-step process in which clusters of node precursors appear on the embryo surface as overlying endoderm cells are removed. We present additional SEM and confocal microscopy studies that help define the transition stages during node morphogenesis. After the initiation of left-sided signaling, the notochordal plate, which is contiguous with the node, generates a barrier at the embryonic midline that restricts the cascade of gene expression to the left side of the embryo. The field is now poised to dissect the genetic and cellular mechanisms that create and organize the specialized cells of the node and midline that are essential for left,right asymmetry. Developmental Dynamics 237:3464,3476, 2008. © 2008 Wiley-Liss, Inc. [source] Tissue surface tensions guide in vitro self-assembly of rodent pancreatic islet cellsDEVELOPMENTAL DYNAMICS, Issue 8 2007Dongxuan Jia Abstract The organization of endocrine cells in pancreatic islets is established through a series of morphogenetic events involving cell sorting, migration, and re-aggregation processes for which intercellular adhesion is thought to play a central role. In animals, these morphogenetic events result in an islet topology in which insulin-secreting cells form the core, while glucagon, somatostatin, and pancreatic polypeptide-secreting cells segregate to the periphery. Isolated pancreatic islet cells self-assemble in vitro into pseudoislets with the same cell type organization as native islets. It is widely held that differential adhesion between cells of the pancreatic islets generates this specific topology. However, this differential adhesion has never been rigorously quantified. In this manuscript, we use tissue surface tensiometry to measure the cohesivity of spherical aggregates from three immortalized mouse pancreatic islet cell lines. We show that, as predicted by the differential adhesion hypothesis, aggregates of the internally segregating INS-1 and MIN6 beta-cell lines are substantially more cohesive than those of the externally segregating ,-TC line. Furthermore, we show that forced overexpression of P-cadherin by ,-TC cells significantly perturbs the sorting process. Collectively, the data indicate that differential adhesion can drive the in vitro organization of immortalized rodent pancreatic islet cells. Developmental Dynamics 236:2039,2049, 2007. © 2007 Wiley-Liss, Inc. [source] A green to red photoconvertible protein as an analyzing tool for early vertebrate developmentDEVELOPMENTAL DYNAMICS, Issue 2 2007Stephan A. Wacker Abstract Lineage labeling is one of the most important techniques in developmental biology. Most recently, a set of photoactivatable fluorescent proteins originating from marine cnidarians became available. Here, we introduce the application of the green to red photoconvertible protein EosFP as a novel technique to analyze early vertebrate development. Both injection of EosFP mRNA and purified, recombinant EosFP followed by a light-driven green to red conversion allow lineage labeling in virtually any temporal and spatial dimension during embryonic development for at least 2 weeks. Specific staining of cells from nonsurface layers is greatly facilitated by light-driven conversion of EosFP compared with traditional methods. Therefore, green to red photoactivatable proteins promise to be a powerful tool with the potential to satisfy the increasing demand for methods enabling detailed phenotypical analyses after manipulations of morphogenetic events, gene expression, or signal transduction. Developmental Dynamics 236:473,480, 2007. © 2006 Wiley-Liss, Inc. [source] Graphic and movie illustrations of human prenatal development and their application to embryological education based on the human embryo specimens in the Kyoto collectionDEVELOPMENTAL DYNAMICS, Issue 2 2006Shigehito Yamada Abstract Morphogenesis in the developing embryo takes place in three dimensions, and in addition, the dimension of time is another important factor in development. Therefore, the presentation of sequential morphological changes occurring in the embryo (4D visualization) is essential for understanding the complex morphogenetic events and the underlying mechanisms. Until recently, 3D visualization of embryonic structures was possible only by reconstruction from serial histological sections, which was tedious and time-consuming. During the past two decades, 3D imaging techniques have made significant advances thanks to the progress in imaging and computer technologies, computer graphics, and other related techniques. Such novel tools have enabled precise visualization of the 3D topology of embryonic structures and to demonstrate spatiotemporal 4D sequences of organogenesis. Here, we describe a project in which staged human embryos are imaged by the magnetic resonance (MR) microscope, and 3D images of embryos and their organs at each developmental stage were reconstructed based on the MR data, with the aid of computer graphics techniques. On the basis of the 3D models of staged human embryos, we constructed a data set of 3D images of human embryos and made movies to illustrate the sequential process of human morphogenesis. Furthermore, a computer-based self-learning program of human embryology is being developed for educational purposes, using the photographs, histological sections, MR images, and 3D models of staged human embryos. Developmental Dynamics 235:468,477, 2006. © 2005 Wiley-Liss, Inc. [source] Differential expression of p120 catenin in glial cells of the adult rat brainTHE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 1 2004Norbert Chauvet Abstract p120 catenin (p120ctn) is involved in the regulation of cadherin-mediated adhesion and the dynamic organization of the actin cytoskeleton by modulating RhoGTPase activity. We have previously described the distribution of p120ctn during rat brain development and provided substantial evidence for the potential involvement of p120ctn in morphogenetic events and plasticity in the central nervous system. Here, we analyzed the cellular and ultrastructural distribution of p120ctn in glial cells of the adult rat forebrain. The highest intensity of immunostaining for p120ctn was found in cells of the choroid plexus and ependyma and was mainly restricted to the plasma membrane. However, p120ctn was almost absent from astrocytes. In contrast, in tanycytes, a particular glial cell exhibiting remarkable morphological plasticity, p120ctn, was localized at the plasma membrane and also in the cytoplasm. We show that a large subpopulation of oligodendrocytes expressed multiple isoforms, whereas other neural cells predominantly expressed isoform 1, and that p120ctn immunoreactivity was distributed through the cytoplasm and at certain portions of the plasma membrane. Finally, p120ctn was expressed by a small population of cortical NG2-expressing cells, whereas it was expressed by a large population of these cells in the white matter. However, in both regions, proliferating NG2-positive cells consistently expressed p120ctn. The expression of p120ctn by cells of the oligodendrocyte lineage suggests that p120ctn may participate in oligodendrogenesis and myelination. Moreover, the expression of p120ctn by various cell types and its differential subcellular distribution strongly suggest that p120ctn may serve multiple functions in the central nervous system. J. Comp. Neurol. 479:15,29, 2004. © 2004 Wiley-Liss, Inc. [source] Generation of branched actin networks: assembly and regulation of the N-WASP and WAVE molecular machinesBIOESSAYS, Issue 2 2010Emmanuel Derivery Abstract The Arp2/3 complex is a molecular machine that generates branched actin networks responsible for membrane remodeling during cell migration, endocytosis, and other morphogenetic events. This machine requires activators, which themselves are multiprotein complexes. This review focuses on recent advances concerning the assembly of stable complexes containing the most-studied activators, N-WASP and WAVE proteins, and the level of regulation that is provided by these complexes. N-WASP is the paradigmatic auto-inhibited protein, which is activated by a conformational opening. Even though this regulation has been successfully reconstituted in vitro with isolated N-WASP, the native dimeric complex with a WIP family protein has unique additional properties. WAVE proteins are part of a pentameric complex, whose basal state and activated state when bound to the Rac GTPase were recently clarified. Moreover, this review attempts to put together diverse observations concerning the WAVE complex in the conceptual frame of an in vivo assembly pathway that has gained support from the recent identification of a precursor. [source] Genetic factors in congenital heart malformationCLINICAL GENETICS, Issue 6 2008G Andelfinger Congenital heart disease is the commonest malformation in humans and contributes greatly to the burden of disease in infancy. Increasingly, developmental origins are also implicated in heart disease in adults. Significant advances have been made over the past decade in elucidating morphogenetic events of heart formation and their underlying molecular cascades, mostly in animal models. Clinical studies are increasingly successful in quantifying and unraveling genetic factors. This review focuses on recent progress made in understanding the genetic underpinnings of normal and abnormal heart formation and highlights the importance of understanding these mechanisms to improve patient management. [source] Taking it to the max: The genetic and developmental mechanisms coordinating midfacial morphogenesis and dysmorphologyCLINICAL GENETICS, Issue 3 2004TC Cox The rapid proliferative expansion and complex morphogenetic events that coordinate the development of the face underpin the sensitivity of this structure to genetic and environmental insult and provide an explanation for the high incidence of midfacial malformation. Most notable of these malformations is cleft lip with or without cleft palate (CLP) that, with an incidence of between one in 600 and one in 1000 live births, is the fourth most common congenital disorder in humans. Despite the obvious global impact of the disorder and some recent progress in identifying causative genes for some prominent syndromal forms, our knowledge of the key genetic factors contributing to the more common isolated cases of CLP is still remarkably patchy. The current understanding of the molecular and cellular processes that orchestrate morphogenesis of the midface, with emphasis on events leading to fusion of the lip and primary palate, is detailed in this review. The roles of crucial factors identified from relevant animal model systems, including BMP4 and SHH, and the likely events perturbed by key genes pinpointed in human studies [such as PVRL1, IRF6p63, MID1, MSX1, and PTCH1] are discussed in this light. New candidates for human CLP genes are also proposed. [source] | ||||||||||