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At least 721 records · Page 40Linked to original sources
PubMed1999

Evidence that MRas1 and MRas3 proteins are associated with distinct cellular functions during growth and morphogenesis in the fungus Mucor racemosus.

The filamentous fungus Mucor racemosus provides a simple and unique model system for defining the function of individual ras genes in a gene family which is closely related to mammalian ras genes. The current study was designed to investigate the role of Mras1 and Mras3 in different stages of fungal morphogenesis, including sporangiospore germination, sporulation, and dimorphic transitions. The overall patterns of Mras1 and Mras3 transcript and protein accumulation were markedly different but, in general, transcripts and proteins were present at low levels during spherical growth and their accumulated level increased severalfold during polar growth (germ tube emergence and elongation). In contrast to Mras1, relatively high levels of Mras3 transcript accumulated during sporulation and MRas3 protein accumulated in sporangiospores. Transformation of M. racemosus with an activated allele of Mras3 reduced growth rate during aerobic sporangiospore germination, while a dominant-negative allele of Mras3 caused a 40% decrease in viable asexual spores. An activated allele of Mras1 increased growth rate during sporangiospore germination but neither activated nor dominant-negative alleles of Mras1 affected total number of asexual spores. Expression of MRas3 and MRas1 proteins appear to be subject to different regulatory mechanisms: exogenous dibutyryl-cAMP and fusidienol caused a strong repression of the level of MRas3 protein (but not MRas1) concurrent with the inhibition of polar growth. Differential posttranslational modification and intracellular localization of MRas1 and MRas3 proteins were also observed. The data strongly suggest that Mras3 and Mras1 play different roles in regulation of cell growth and morphogenesis in Mucor.

Alkyl and Aryl Transferases↗
PubMed2002

Control of embryonic lung branching morphogenesis by the Rho activator, cytotoxic necrotizing factor 1.

BACKGROUND: Lung development is sensitive to physiological stresses, and its development may be impaired by physical distortion, as in patients with congenital diaphragmatic hernia. Yet, little is known about how mechanical forces can influence lung morphogenesis. Studies with cultured cells suggest that cytoskeletal tension may play a key role in growth control. Since the small GTPase Rho plays an important role in the control of cell tension generation, we carried out studies to test the hypothesis that changes in Rho-mediated cell tension may influence branching morphogenesis. METHODS: Embryonic lung buds from timed pregnant Swiss Webster mice were microdissected on Embryonic Day 12 (E12), and whole organs were cultured in serum-free medium in the presence of the Rho activator cytotoxic necrotizing factor 1 (CNF-1) for 48 h. Serial measurements of the degree of epithelial branch formation and tissue maturation were performed using light microscopy and computerized image analysis. RESULTS: At 48 h, embryonic lungs treated with 2 ng/ml CNF-1 increased their terminal bud count by 236 +/- 18% (P = 0.01) compared with 132 +/- 2% for untreated controls. However, dose-response experiments revealed biphasic behavior: at a higher dose of CNF-1 (200 ng/ml), bud number was actually decreased relative to controls (43 +/- 1%, P < 0.001). Histological analysis revealed that individual glands appeared to be more highly developed at low-dose CNF-1, whereas the high dose produced gland contraction. CONCLUSIONS: These data support a potential role for Rho and cytoskeletal tension in control of epithelial pattern formation during lung development.

Animals↗
PubMed1993

Is morphogenesis an intrinsically robust process?

Because morphogenesis is dynamically complex, involving many processes operating over different spatial and temporal scales, it is generally assumed that the stability and repeatability of development depends primarily upon accurate control over parameter values i.e. a precise genetic program. However, it is possible that the dynamic coupling between the different mechanisms involved in development reduces the choices available to the system because of bias in successive symmetry-breaking events. Evidence for such stable cascades in morphogenetic processes is described, and a general argument is presented for morphogenesis as an intrinsically robust process. The evolutionary implications of the hypothesis are considerable.

Acetabularia↗
PubMed1997

A dynamic model for the morphogenesis of the late vertebrate lens.

A mathematical model is presented for the morphogenesis of the post-vesicular vertebrate lens with an umbilical suture. The lens is modeled as having four compartments: anterior epithelium (germinative and central anterior zones), recruitment zone (transitional zone), cortex (discrete concentric cohorts of secondary cortex fiber cells, each cohort treated individually), and nucleus. Equations are written to describe the time evolution of the cohorts; their shapes collectively determine the shape of the lens. The growth of cell volume is exponential, with different rates in the cortex and epithelium; recruitment of epithelium cells into the cortex is described as resulting from an overproduction of epithelial basal (capsular) surface in the anterior epithelium. The equations contain three dimensionless numbers determined by the physiology of the epithelium and cortex cells. Solutions are stable attractors in a morphological space. All solutions entail exponential growth of the lens diameter; a portion of parameter space corresponds to exponential growth superimposed on large amplitude oscillations in lens shape. Emergent time-scales for increase in lens size and oscillation period are an order of magnitude longer than the cellular growth time-scales. The lens shapes tend to a family of stable scaling solutions, the shapes of which remain unchanged as the lens grows. The model is applied to morphological data for the chick and lamprey lenses. The dynamics described are seen as exemplifying an auto-regulatory morphogenesis process wherein a system passes through a sequence of developmental stages. Each stage is characterized by its own fixed informing geometry (a set of defining spatial relationships), within which a growth process unfolds autonomously, generating a dynamically stable structure. The developing system invokes a means of forgetting dated structural information; this dissipation is necessary to the pattern formation process.

Animals↗
PubMed1999

Seeking a regulatory roadmap for heart morphogenesis.

Despite descriptive studies spanning centuries, we are still lacking an integrated concept of how molecular patterning information is developed in the heart, and how this information guides morphogenesis. With an increasing number of regionally-expressed cardiac genes and transgenes being identified, along with new animal models of cardiac dysmorphogenesis and an exciting array of genetic tools for further dissection, the need for an integrated morphogenetic concept is acute. Models invoking a linear array of cardiac segments are difficult to reconcile with the observation that those segments are evident only on the outer curvature of the heart tube. Molecular and anatomical evidence supports the view that chamber specification is achieved by interpretation of dorso-ventral (inner curvature/outer curvature), as well as anterior-posterior patterning information in the primary heart tube. In this essay, I examine some of the issues influencing and perhaps confusing our view of cardiac morphogenesis and briefly discuss regulatory genes in the context of an evolving morphogenetic model.

Animals↗
PubMed2001

Inhibition of axonal morphogenesis by nonlethal, submicromolar concentrations of methylmercury.

We investigated the effects of sublethal concentrations of the neurotoxicant methylmercury (MeHg) on the developmental progression of cultured neurons to the stage of axonal morphogenesis. Chick (E8) forebrain neurons in vitro develop axons by a stereotyped developmental sequence nearly identical to that of widely used rat hippocampal neurons, but at much less cost and difficulty. In this chick forebrain system, 40% of neurons develop long axons after 2 days in culture, and 80% have axons after 4 days. A single, 2-h exposure to 0.5 or 0.25 microM MeHg reduced the number of neurons developing axons to approximately half that of controls without causing significant cell death for at least 2 days after treatment. Although MeHg caused an immediate depolymerization of neuronal microtubules, after 1 day of recovery the microtubule array of MeHg-treated neurons was indistinguishable by immunofluorescent assay from that of untreated cells at equivalent development stages. Thus, the inhibition of axonal development by submicromolar concentrations of MeHg did not appear to be the direct effect of microtubule disassembly. Chelation of Ca(2+) during MeHg exposure appeared to exert a small immediate protective effect, as previously reported, but was itself toxic within 1 day after chelation. We suggest that this inhibition of axonal morphogenesis by acute, sublethal concentrations of MeHg may play a role in the developmental syndrome caused by environmental exposure to MeHg.

Animals↗
PubMed2006

Early steps in avian reovirus morphogenesis.

Avian reoviruses are important pathogens that may cause considerable economic losses in poultry farming. Their genome expresses at least eight structural and four nonstructural proteins, three of them encoded by the S1 gene. These viruses enter cells by receptor-mediated endocytosis, and acidification of virus-containing endosomes is necessary for the virus to uncoat and release transcriptionally active cores into the cytosol. Avian reoviruses replicate within cytoplasmic inclusions of globular morphology, termed viral factories, which are not microtubule-associated, and which are formed by the nonstructural protein muNS. This protein also mediates the association of some viral proteins (but not of others) with inclusions, suggesting that the recruitment of viral proteins into avian reovirus factories has specificity. Avian reovirus morphogenesis is a complex and temporally controlled process that takes place exclusively within viral factories of infected cells. Core assembly takes place within the first 30 min after the synthesis of their protein components, and fully formed cores are then coated by outer-capsid polypeptides over the next 30 min to generate mature infectious reovirions. Based on data from avian reovirus studies and on results reported for other members of the Reoviridae family, we present a model for avian reovirus gene expression and morphogenesis.

Animals↗
PubMed2006

Reovirus structure and morphogenesis.

Assembly of a mature infectious virion from component parts is one of the last steps in the replicative cycle of most viruses. Recent advances in delineating aspects of this process for the mammalian orthoreoviruses (MRV), nonenveloped viruses composed of a genome of ten segments of double-stranded RNA enclosed in two concentric icosahedral protein capsids, are discussed. Analyses of temperature-sensitive (ts) assembly-defective reovirus mutants have been used to better understand requirements for viral inclusion formation and capsid morphogenesis. Newly determined high-resolution structures of virtually all MRV proteins, combined with complete MRV genomic sequence information and elucidation of sequence lesions in ts mutants, is now providing a context for molecularly understanding interactions that promote, or abrogate, reovirus capsid assembly. Additional advances in understanding required signals for whole genome construction from sets of the ten individual genes, and in transcapsidation of subviral particles with engineered outer capsid proteins, provide additional molecular genetic understanding of reovirus protein structure-function and morphogenesis.

Capsid↗
PubMed1993

Onset of gastrulation, morphogenesis and somitogenesis in mouse embryos displaying compensatory growth.

This is a study on the ability of mouse embryos to compensate for a loss of cells and to develop with body parts of normal size and normal proportions during post-implantation development. Micro-manipulations were performed on 4-cell pre-implantation mouse embryos to reduce the number of cells by 25% (3/4 embryos) or 50% (2/4 embryos). Blastocysts developed from these embryos showed a preferential loss of inner cell mass population, and fewer of them formed viable embryos after implantation. The size of post-implantation 3/4 embryos was initially smaller than controls of the same gestational age, but compensatory growth, achieved by increasing cell numbers at above the normal rate and beyond the normal duration, took place between 6.5 and 11.5 days, resulting in a complete restoration of body size. During compensatory growth the 3/4 embryos rescheduled events of gastrulation and morphogenesis in keeping with cell number or body size appropriate for each developmental stage. The formation of the correct number of somites was accomplished by changing the rate of somite segmentation and by an adjustment of the size of individual somites and somitomeres proportional to the available amount of precursor tissues. Morphogenesis and pattern formation in embryos recovering from earlier cell losses are therefore regulated in accordance to tissue volume (or cell number) instead of chronological age or some intrinsic cellular clock.

Animals↗
PubMed1996

Regional differences in morphogenesis of the neuroepithelium suggest multiple mechanisms of spinal neurulation in the mouse.

A study of neuroepithelial morphogenesis in the mouse embryo has identified three modes of neural tube formation that occur consecutively as neurulation progresses along the spinal region. The three modes of neurulation differ in the extent to which the neuroepithelium exhibits formation of "hinge points', i.e. localised bending owing to reduction in apical surface area. In Mode 1, bending occurs only in the neuroepithelium overlying the notochord, creating a median hinge point. The neural folds remain straight along both apical and basal surfaces, resulting in a neural tube with a slitshaped lumen. In Mode 2, the neuroepithelium forms paired dorsolateral hinge points, as well as a median hinge point, whereas the remaining portions of the neuroepithelium do not bend. This produces a neural tube with a diamond-shaped lumen. In Mode 3 neurulation, the entire neuroepithelium exhibits bending, so that the cells specific hinge points are not discernible; the resulting neural tube has a circular lumen. The three modes of neurulation are present in all three strains of mice studied: C57BL/6, CBA/Ca and curly tail, a mutant predisposed to neural tube defects. However, curly tail embryos exhibit a delay in transition from Mode 2 to Mode 3, preceding faulty closure of the posterior neuropore. This heterogeneity of neurulation morphogenesis in the mouse embryo indicates that the underlying mechanisms may vary along the body axis. Specifically, we suggest that Mode 1 neurulation is driven largely by forces generated extrinsic to the neuroepithelium, in adjacent tissues, whereas Mode 3 neurulation is dependent primarily on forces generated intrinsic to the neuroepithelium. Down the body axis, there is a gradual decrease in the area of ectoderm involved in neural induction and, as neurulation reaches lower spinal levels, the newly induced neural plate exhibits marked indentation from the time of its first appearance. The transition from primary neurulation (neural folding of Mode 3 type) to secondary neurulation (neural tube formation by cavitation) appears to be a smooth continuation of this trend, with loss of contact between the newly induced neuroepithelium and the outside of the embryo.

Animals↗
PubMed1976

Morphogenesis of the spinal canal, normal and stenotic.

The closest formative developmental dependence of the axial skeleton upon the morphogenesis of the intraspinal nervous structures is reflected in the roentgen features of the individual vertebrae as well as of the vertebral column in its entirety. The vertebroneural developmental events are characterized by a steady relative decrease in size of the nervous structures (the first to be laid down and huge in the embryonic period) under a corresponding increase in size of the skeletogenic tissues. There exists experimental evidence that the maintenance of the necessary developmental balance between the two tissues, the bony and the skeletogenic, is a function of the nervous substance. The tight spinal canal appears to result from a failure of the latter neural function leading to overgrowth of the bony structures, viz., to massive vertebrae and laminae encroaching upon the neural contents. Morphogenesis of the normal and tight lumbar spinal canal is discussed with special reference to the developmental interrelations between the cauda equina complex and the lumbar vertebrae.

Constriction↗
PubMed1985

Errors of morphogenesis and inborn errors of immunity 20 years after the discovery of DiGeorge anomaly.

The heuristic concept of "inborn errors of metabolism" was introduced more then 70 years ago and by analogy has prompted the more recent introduction of the term "inborn errors of immunity". It is now well recognized that many inborn errors of immunity can be considered inborn errors of metabolism. Typically, many forms of severe combined immunodeficiency result from adenosine deaminase deficiency, i.e., an inborn error of purine metabolism. On the other hand, errors of immunity are often associated with "errors of morphogenesis", resulting from an intrinsically abnormal developmental process (malformation), a secondary or extrinsic interference with originally normal development (disruption), or an abnormal organization of cells into tissues (dysplasia). Twenty years after the original description, the DiGeorge anomaly should be considered an inborn error of morphogenesis and immunity due either to disruption or less frequently to malformation. In other immunodeficiencies, such as ataxia telangiectasia, the morphologic and immunologic errors result from a dyshistogenesis, i.e., dysplasia. Also, true malformation syndromes, such as Down's syndrome, are consistently associated with immunodeficiency.

Animals↗
PubMed1991

Relationship between appearance of GABA, fluorogenic monoamines and cytochrome oxidase activity during prenatal morphogenesis of chick myenteric plexus.

The basic histology of the developing embryonic gut wall of the chick was examined on haematein and eosin-stained paraffin sections. In parallel with this, the ontogenic sequence of myenteric plexus formation was followed on whole mounts after NADH diaphorase histochemistry. The presence of nerve elements was verified also by electron microscopy. The appearance of enteric gamma-aminobutyric acid-containing neurons, as an example of an intrinsic inhibitory neuronal system, was studied by using an antiserum against the gamma-aminobutyric acid glutaraldehyde bovine serum albumin conjugate. The development of noradrenergic innervation as an extrinsic inhibitory supply was followed by means of a glyoxylic acid-induced fluorescence method. Cytochrome oxidase activity was detected histochemically. Three consecutive steps of the morphogenesis of the myenteric plexus were revealed; first the appearance of a cellular crest at the mesenteric border on embryonic day 9; second the migration and clustering of nerve cells between embryonic days 10 and 16; then the elongation of neurites on embryonic days 16 and 21. Immunoreactive and also fluorescent fibres were first detected on the 14th day of incubation, while immunopositive cell bodies appeared only after hatching. In the early stages the cytochrome oxidase activity was restricted to the perikarya, while at the end of embryonic development the activity also appeared in the ganglionic neuropile. On the basis of these observations, we concluded that there is a close time relation between the morphogenesis and the biochemical and functional maturation of the myenteric plexus.

Animals↗
PubMed1992

Morphogenesis of African swine fever virus in monkey kidney cells after reversible inhibition of replication by cycloheximide.

The late cytoplasmic phases of African swine fever virus (ASFV) morphogenesis in monkey kidney cells have been studied by transmission electron microscopy, focusing attention on the synthesis of viral envelopes. Morphogenesis was studied after reversible cycloheximide blockage of monkey kidney cells infected with ASFV. ASFV appears to synthesize its external and internal envelopes within the cellular cytoplasm, at the same time as the capsid is formed, with intracellular and extracellular virions showing similar structure and polypeptide composition.

African Swine Fever Virus↗
PubMed1980

Morphogenesis and structure of caprine respiratory syncytial virus.

Cell cultures inoculated with caprine respiratory syncytial virus (RSV) were studied with light, fluorescent, and electron microscopy to determine the morphogenesis and structure of the virus. Small syncytia were seen after 36 hours in culture. After 48 hours in culture, syncytia were large and numerous and pleomorphic cytoplasmic inclusions were seen. These inclusions were more pronounced and numerous later in the infection cycle. Indirect immunofluorescence revealed a diffuse to granular cytoplasmic fluorescence with fluorescing fibrils on the cell surface. With the electron microscope, filamentous (100-160 nm) and spherical (90-160 nm) particles were seen budding off the cell membrane. The number of virus buds diminished with increased size of syncytia. Granular pleomorphic cytoplasmic inclusions were seen near the nucleus, and electron dense masses were seen just beneath the cytoplasmic membrane where large quantities of virus were budding from the cell surface. The first type of inclusion had distinct borders; the second diffuse borders and appeared to contain viral nucleoprotein. Negative staining revealed spherical, pleomorphic, and filamentous forms of the virus; the last form predominated. The virions were covered with club-shaped projections, and the nucleocapsids were seen as fragile strands frequently broken into fragments or as isolated rings. Morphogenesis and structure of the caprine RSV places this virus with the Pneumovirus genus of the Paramyxoviridae family.

Animals↗
PubMed1978

Morphogenesis of the nodamura virus in the larbae of the lepidopteran Galleria mellonella (L.).

The pathogenesis and morphogenesis of the Nodamura virus, an insect picorna- virus which can also infect vertebrates such as newborn mice, are described in the larvae of G. mellonella. Examination of thin sections of muscle, salivary and moulting glands, hemocytes adipose tissue and hypodermis of the infected larvae of G. mellonella shows in the cytoplasm the accumulation of viral particles either dispersed or in a stringlike or paracrystalline array. These arrays of virions can be within membrane- bound vesicles. Helical filaments of 110 A of diameter can be observed inside the basal membranes and later in the cytoplasm, in relation to the infection of muscular or adipose tissues. The morphogenesis of Nodamura virus in G. mellonella or in suckling mice is very similar to that of the Coxsackie A virus observed in the mouse.

Animals↗
PubMedDate not supplied

Preliminary evidence for a cholinergic-like system in lichen morphogenesis.

Membrane acetylcholinesterase activity is considered to be a marker for a cholinergic system. When temporarily expressed in differentiating cells other than the nervous or muscular ones, it may play a role in morphogenesis. In the lichen Parmelia caperata (L.) Ach., acetylcholinesterase is histochemically localized mainly in the cell walls and/or membranes of both symbionts just where they proliferate and form well-organized propagation structures, the soredia. The enzyme activity is first detected in a few algae undergoing aplanosporogenesis and later in medullary hyphae that reach the dividing algae by elongating perpendicularly to the thallus surface. This histochemical pattern that is associated with algal proliferation and oriented hyphal growth is characteristic of early morphogenesis of the soredia; when fully differentiated, they consist of an inner dividing alga and an outer hyphal envelope, both showing cholinesterase activity. Substrate specificity and inhibitor sensitivity of the histochemical staining indicate an acetylcholinesterase-like activity. However, extracts of the thallus areas where soredia develop give four bands of cholinesterase activity on disc electrophoresis: the two cathodal bands have the characteristics of acetylcholinesterase, the others of pseudocholinesterase. One of the latter hydrolyses propionylthiocholine very rapidly. The findings suggest that in lichen symbiosis, a cholinergic-like system participates in regulating morphogenetic processes such as cell division, oriented tip growth and alga-fungus membrane interactions. Environmental stimuli, particularly light, might trigger the development of soredia by modulating the activity of the cholinergic mechanism.

Acetylcholinesterase↗
PubMed1987

Transient appearance of and regional differences in apical cell surface materials during early morphogenesis of the chicken lens.

Apical cell surface materials were analysed with staining and lectin histochemistry in the chicken lens, from the earliest stages of lens morphogenesis through the completion of primary fibre cell elongation. Acidic materials were found to accumulate on the apical cell surface of the presumptive lens fibres from the mid cup stage through the early stages of lens vesicle formation, peaking just before lens fibre cell elongation. These materials labelled strongly with concanavalin A, but not with soybean lectin. By the completion of fibre cell elongation, these materials were gone. Conversely, the apical surface of the future lens epithelial cells demonstrated neutral materials, which were also largely removed by the completion of primary fibre cell elongation. These materials labelled with both concanavalin A and soybean lectin. The identity of these materials is not known, but their location prior to and during chicken lens morphogenesis suggests that they may be involved in establishing polarity during elongation of the primary lens fibre cells.

Animals↗