Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “morphogenesis”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 811 records · Page 45Linked to original sources
PubMed1998

Confocal laser scanning microscopic study [corrected] of tartrate-resistant acid phosphatase-positive cells in the dental follicle during early morphogenesis of mouse embryonic molar teeth.

Tartrate-resistant acid phosphatase (TRAPase)-positive cells were examined during the early morphogenesis of mouse mandibular first molar teeth, using a simultaneous azo dye-coupling technique and confocal laser scanning microscopy (CLSM). CLSM of paraffin-embedded sections revealed that cells exhibiting TRAPase fluorescence appeared along the marginal region of the condensed dental mesenchyme, not yet the dental follicle, at embryonic day 12 (E12). The follicle was recognized histologically as a population of fibroblastic cells in tooth organs at E14, and TRAPase-positive cells were localized among the follicular cells. Light-microscopic observations of microsliced thick sections showed the overall morphology of the TRAPase-positive cells. A few positive cells of E13 tooth organs were oval, and the intense reaction products of TRAPase revealed complex processes on positive cells in E14 tooth organs. Three-dimensional fluorescent images of TRAPase-positive cells using microsliced sections and CLSM showed their unique morphology of long processes with small spine-like projections at E14. Thus, TRAPase-positive cells appeared in the region of the prospective follicle at the bud stage (E12 and 13) before the formation of the follicle proper. In addition, the formation of the follicle and the appearance of TRAPase-positive cells with unique morphology were correlated in their developmental stage (E14). The findings suggest that the TRAPase-positive cells may be involved in the formation of the dental follicle in early tooth morphogenesis.

Acid Phosphatase↗
PubMed2003

ADAM 10: an active metalloprotease expressed during avian epithelial morphogenesis.

The ADAMs are a family of proteins containing multiple functional domains. We have cloned the avian orthologue of ADAM 10 and demonstrate that it has metalloprotease activity. Chick ADAM 10 is expressed in the developing dermatome and myotome of the somite, epidermis, gut endoderm, the epithelial tissues of the kidney, liver, and heart, and in neural crest cells. The expression patterns and protein distribution of ADAM 10 suggest it may play a significant role in the morphogenesis of several epithelial tissues. When a dominant-negative metalloprotease-mutant form of ADAM 10 is expressed in the ectoderm or ADAM 10 expression is knocked down with morpholinos, morphogenesis and tissue specification are altered.

Amino Acid Sequence↗
PubMed2003

Temporal effects of Sprouty on lung morphogenesis.

Paracrine signaling mediated by FGF-10 and the FGF-R2IIIb receptor is required for formation of the lung. To determine the temporal requirements for FGF signaling during pulmonary morphogenesis, Sprouty-4 (Spry-4), an intracellular FGF receptor antagonist, was expressed in epithelial cells of the fetal lung under control of a doxycycline-inducible system. Severe defects in lobulation and severe lung hypoplasia were observed when Spry-4 was expressed throughout fetal lung development (E6.5-E18.5) or from E6.5 until E13.5. Effects of Spry-4 on branching were substantially reversed by removal of doxycycline from the dam at E12.5, but not at E13.5. In contrast, when initiated late in development (E12.5 to birth), Spry-4 caused less severe pulmonary hypoplasia. Expression of Spry-4 from E16.5 to E18.5 reduced lung growth and resulted in perinatal death due to respiratory failure. Expression of Spry-4 during the saccular and alveolar stages, from E18.5 to postnatal day 21, caused mild emphysema. These findings demonstrate that the embryonic-pseudoglandular stage is a critical time period during which Spry-sensitive pathways are required for branching morphogenesis, lobulation, and formation of the peripheral lung parenchyma.

Animals↗
PubMed2003

Heparan sulfate-FGF10 interactions during lung morphogenesis.

Signaling by fibroblast growth factor 10 (FGF10) through FGFR2b is essential for lung development. Heparan sulfates (HS) are major modulators of growth factor binding and signaling present on cell surfaces and extracellular matrices of all tissues. Although recent studies provide evidence that HS are required for FGF-directed tracheal morphogenesis in Drosophila, little is known about the HS role in FGF10-mediated bud formation in the vertebrate lung. Here, we mapped HS expression in the early lung and we investigated how HS interactions with FGF10-FGFR2b influence lung morphogenesis. Our data show that a specific set of HS low in O-sulfates is dynamically expressed in the lung mesenchyme at the sites of prospective budding near Fgf10-expressing areas. In turn, highly sulfated HS are present in basement membranes of branching epithelial tubules. We show that disrupting endogenous gradients of HS or altering HS sulfation in embryonic lung culture systems prevents FGF10 from inducing local responses and markedly alters lung pattern formation and gene expression. Experiments with selectively sulfated heparins indicate that O-sulfated groups in HS are critical for FGF10 signaling activation in the epithelium during lung bud formation, and that the effect of FGF10 in pattern is in part determined by regional distribution of O-sulfated HS. Moreover, we describe expression of a HS 6-O-sulfotransferase preferentially at the tips of branching tubules. Our data suggest that the ability of FGF10 to induce local budding is critically influenced by developmentally regulated regional patterns of HS sulfation.

Animals↗
PubMed2003

PEA3 transcription factors are expressed in tissues undergoing branching morphogenesis and promote formation of duct-like structures by mammary epithelial cells in vitro.

The genetic program that controls reciprocal tissue interactions during epithelial organogenesis is still poorly understood. Erm, Er81 and Pea3 are three highly related transcription factors belonging to the Ets family, within which they form the PEA3 group. Little information is yet available regarding the function of these transcription factors. We have previously used in situ hybridization to compare their expression pattern during critical stages of murine embryogenesis [Oncogene 15 (1997), 937; Mech. Dev. 108 (2001), 191]. In this study, we have examined the expression of PEA3 group members during organogenesis of the lung, salivary gland, kidney, and mammary gland. In all of these developmental settings, we observed a tight correlation between branching morphogenesis and the expression of specific members of the PEA3 group. To assess the functional relevance of these findings, Erm and Pea3 were overexpressed in the TAC-2.1 mammary epithelial cell line, which has the ability to form branching duct-like structures when grown in collagen gels. We found that overexpression of Erm and Pea3 markedly enhances branching tubulogenesis of TAC-2.1 cells and also promotes their invasion into a collagen matrix. Collectively, these findings suggest that the differential expression of PEA3 group transcription factors has an important role in the regulation of branching morphogenesis and raise the question of their implication in branching signaling.

Animals↗
PubMed2003

Optic cup morphogenesis requires pre-lens ectoderm but not lens differentiation.

The formation of the vertebrate optic cup is a morphogenetic event initiated after the optic vesicle contacts the overlying surface/pre-lens ectoderm. Placodes form in both the optic neuroepithelium and lens ectoderm. Subsequently, both placodes invaginate to form the definitive optic cup and lens, respectively. We examined the role of the lens tissue in inducing and/or maintaining optic cup invagination in ovo. Lens tissue was surgically removed at various stages of development, from pre-lens ectoderm stages to invaginating lens placode. Removal of the pre-lens ectoderm resulted in persistent optic vesicles that initiated neural retinal differentiation but failed to invaginate. In striking contrast, ablation of the lens placode gave rise to optic vesicles that underwent invagination and formed the optic cup. The results suggest that: (1) the optic vesicle neuroepithelium requires a temporally specific association with pre-lens ectoderm in order to undergo optic cup morphogenesis; and (2) the optic cup can form in the absence of lens formation. If ectopic BMP is added, a neural retina does not develop and optic cup morphogenesis fails, although lens formation appears normal. FGF-induced neural retina differentiation in the absence of the pre-lens ectoderm is not sufficient to create an optic cup. We hypothesize the presence of a signal coming from the pre-lens ectoderm that induces the optic vesicle to form an optic cup.

Animals↗
PubMed1982

Determinants in the morphogenesis of muscle tendon insertions.

The factors that normally determine the location and insertion of a muscle were explored in human experiments of nature with early problems in morphogenesis. Monozygotic conjoined twins for whom there could be no genetic determinants for muscle attachments at the sites of juncture served as one model; these attachments had to follow general principles of morphogenesis. A second type of problem involved absence of bone that presumably antedated muscle and tendon development (e.g., genetically determined radial aplasia). A third category included mechanical alteration of early limb position that may have occurred prior to the development of muscle attachments (e.g., early amnion rupture sequence). The dissection findings from all three types imply a general hierachy of muscle tendon attachments. Tendons appear to attach preferentially to bone. In the absence of the bone to which they would normally attach, they will attach to the next closest bone. If no such bone is available, tendons may attach to other tendons; and if no tendons is available, occasionally they will attach to the fascia of another muscle. If there is no connective tissue attachment site, there will be no muscle, implying a need for function in the development and preservation of muscle.

Abnormalities, Multiple↗
PubMed1991

Generative rules for the morphogenesis of epithelial tubes.

A finite elements model imitating the morphogenesis of smoothly curved tubular epithelial rudiments is suggested. It is based upon the experimentally proved assumption of the lateral (tangential) pressure between adjacent epithelial cells. The main idea of the model is that under a non-zero local curvature the lateral cell-cell pressure acquires the radial components which are absent under zero curvature. In the framework of the model we investigate the roles of initial geometry, the different coefficients relating the local curvatures and radial cell shifts, and of visco-elastical cell-cell linkages in the shaping process. We also employ the different temporal regimes (both periodical and constant) of the lateral pressure exerted and the different overall durations of the modelling. As a result, we get a set of biologically realistical shapes, almost all of them belonging to the same basical "trefoiled" archetype. Among the variables explored, shaping was most affected by the changes in visco-elastical coefficients, in the temporal regimes and in the overall duration of the modelling. The model shows that rather complicated and realistical shapes of epithelial rudiments can be obtained without assuming any initial regional differences inside cell layers. The model may be useful for understanding the principles underlying both genetical and epigenetical regulation of the morphogenesis.

Animals↗
PubMed1987

Model of pattern formation in epithelial morphogenesis.

One of the most universal events in morphogenesis is the formation of domains of morphologically polarized cells in the initially homogeneous epithelial sheets. We investigate the possibility of considering this process as a phenomenon of self-organization which is based upon the following experimentally proven mechanochemical cell properties: (1) a capacity of individual cells for morphological polarization considered as a bistable "all-or-none" transition of a cell from a non-polarized to a polarized state; (2) transmission of this capacity from one cell to another on their contacts; (3) feedback relations between co-operative cell polarization and tangential elastic tensions in a cell sheet: cell polarization increases tangential tensions whereas the latter inhibit further cell polarization. We have constructed a phenomenological model which formally expresses the above properties. Its mathematical description includes but few macroscopic parameters available to experimental investigation and controlled changes. The analysis of the collective dynamic regimes of cell polarization demonstrates that variations of some non-specific parameters leads to spontaneous transition in the morphology of cell layers accompanied by symmetry breaking (Turing's instability). Under these conditions either long-range ordered patterns of cell polarization (including hexagonal cell nets) or non-regular spotted structures can emerge. In the particular case of a sheet having fixed complete dimensions and lacking any external elastic bonds a stable macrostate is created; it corresponds to the sheet's binary subdivision into polarized and non-polarized cell domains of size-invariant proportions. The model conclusions are compared with the morphogenetical processes in sea-urchin development, the morphogenesis of skin derivates and artificially induced budding in hydrozoa.

Animals↗
PubMed1983

Thyroid follicular morphogenesis mechanism: organ culture of the fetal gland as an experimental approach.

The morphological and physiological changes induced by organ culture and thyroid-stimulating hormone (TSH) stimulation in the rat fetal thyroid gland were studied. Organ culture increased Golgi activity which was further enhanced by TSH, subsequently facilitating the formation of intracellular lumina. TSH also raised the intracellular cAMP level. The intracellular lumina observed during follicular morphogenesis are structurally comparable to typical intracellular cavities formed in adult thyroid cells, which are considered as being the result of increased Golgi activity. The intracellular lumen, therefore, is probably not a physiologically significant step in thyroid morphogenesis.

Animals↗
PubMed1999

Simulation of vessel morphogenesis using cellular automata.

We present a cellular automaton model, including lateral inhibition of an autocatalytic morphogen, as well as a genetic switch that differentiates tissue into substrate-depleting vessels. This model yields isotropic morphogenesis, including: dichotomous and lateral branching, blind vessel ends, and closed loops due to anastosmosis. The algorithm consists of a list of simple rules describing the essential biophysical features, permitting comfortable programming and fast computations. Depending on the choice of the substrate s, the model is applicable to leaf veins (s is auxin), insect trachea (s is CO2) or neovascularization (s is an angiogenesis factor). Sequential addition of rules can be correlated to evolutionary steps in leaf morphogenesis.

Algorithms↗
PubMed1998

Neural crest development: the interplay between morphogenesis and cell differentiation.

The final pattern of tissues established during embryogenesis reflects the outcome of two developmental processes: differentiation and morphogenesis. Avian neural crest cells are an excellent system in which to study this interaction. In the first phase of neural crest cell migration, neural crest cells separate from the neural epithelium via an epithelial-mesenchymal transformation. We present three models to account for this process: (1) separation by asymmetric mitosis, (2) separation by generating tractional force in order to rupture cell adhesions and (3) loss of expression or function of cell-cell adhesion molecules that keep the presumptive neural crest cells tethered to the neural epithelium. Evidence is presented that the segregation of the neural crest lineage apart from the neural epithelium is caused by the epithelial-mesenchymal transformation. Once they have detached from the neural tube, neural crest cells take two pathways in the trunk of the chick embryo: (1) the ventral path between the neural tube and somite, where neural crest cells give rise to neurons and glial cells of the peripheral nervous systems, and (2) the dorsolateral path between the ectoderm and dermamyotome of the somite, where they differentiate into pigment cells of the skin. We present data to suggest that the migration and differentiation along the ventral path is controlled primarily by environmental cues, which we refer to as the environment-directed model of neural crest morphogenesis. Conversely, only melanoblasts can migrate into the dorsolateral space, and the ability to invade that path is dependent upon their early specification as melanoblasts. We call this the phenotype-directed model for neural crest cell migration and suggest that this latter model for the positioning of neural crest derivatives in the embryo may be more common than previously suspected. These observations invite a re-examination of patterning of other crest derivates, which previously were believed to be controlled by environmental cues.

Animals↗
PubMed2000

Tribbles coordinates mitosis and morphogenesis in Drosophila by regulating string/CDC25 proteolysis.

Morphogenesis and cell differentiation in multicellular organisms often require accurate control of cell divisions. We show that a novel cell cycle regulator, tribbles, is critical for this control during Drosophila development. During oogenesis, the level of tribbles affects the number of germ cell divisions as well as oocyte determination. The mesoderm anlage enters mitosis prematurely in tribbles mutant embryos, leading to gastrulation defects. We show that Tribbles acts by specifically inducing degradation of the CDC25 mitotic activators String and Twine via the proteosome pathway. By regulating CDC25, Tribbles serves to coordinate entry into mitosis with morphogenesis and cell fate determination.

Animals↗
PubMed1998

The VAB-1 Eph receptor tyrosine kinase functions in neural and epithelial morphogenesis in C. elegans.

Mutations in the C. elegans vab-1 gene disrupt the coordinated movements of cells during two periods of embryogenesis. vab-1 mutants are defective in the movement of neuroblasts during closure of the ventral gastrulation cleft and in the movements of epidermal cells during ventral enclosure of the embryo by the epidermis. We show that vab-1 encodes a receptor tyrosine kinase of the Eph family. Disruption of the kinase domain of VAB-1 causes weak mutant phenotypes, indicating that VAB-1 may have both kinase-dependent and kinase-independent activities. VAB-1 is expressed in neurons during epidermal enclosure and is required in these cells for normal epidermal morphogenesis, demonstrating that cell-cell interactions are required between neurons and epidermal cells for epidermal morphogenesis.

Amino Acid Sequence↗
PubMed1999

Vascular endothelial cell adherens junction assembly and morphogenesis induced by sphingosine-1-phosphate.

Vascular endothelial cells undergo morphogenesis into capillary networks in response to angiogenic factors. We show here that sphingosine-1-phosphate (SPP), a platelet-derived bioactive lipid, activates the EDG-1 and -3 subtypes of G protein-coupled receptors on endothelial cells to regulate angiogenesis. SPP induces the Gi/mitogen-activated protein kinase/cell survival pathway and the small GTPase Rho- and Raccoupled adherens junction assembly. Both EDG-1-and EDG-3-regulated signaling pathways are required for endothelial cell morphogenesis into capillary-like networks. Indeed, SPP synergized with polypeptide angiogenic growth factors in the formation of mature neovessels in vivo. These data define SPP as a novel regulator of angiogenesis.

Animals↗
PubMed2003

Tube morphogenesis: making and shaping biological tubes.

Many organs are composed of epithelial tubes that transport vital fluids. Such tubular organs develop in many different ways and generate tubes of widely varying sizes and structures, but always with the apical epithelial surface lining the lumen. We describe recent progress in several diverse cell culture and genetic models of tube morphogenesis, which suggest apical membrane biogenesis, vesicle fusion, and secretion play central roles in tube formation and growth. We propose a unifying mechanism of tube morphogenesis that has been modified to create tube diversity and describe how defects in the tube size-sensing step can lead to polycystic kidney disease.

Animals↗
PubMed1999

Centric diatom morphogenesis: a model based on a DLA algorithm investigating the potential role of microtubules.

Diatoms are single-celled algae which possess characteristic rigid cell walls (frustules) composed of amorphous silica. Frustule formation occurs within a specialised organelle termed the silica deposition vesicle (SDV). During diatom morphogenesis, silica particles are transported to the SDV by silica transport vesicles. Once released within the SDV, the particles are then thought to diffuse until they encounter part of the growing aggregate upon which they adhere. The particles may then undergo a further period of surface relocalisation (sintering) which leads to a smoothing of the surface. A number of computer simulations based on a modified diffusion-limited aggregation (DLA) algorithm, have been undertaken to investigate the potential role of microtubules (which are known to be associated with the periphery of the SDV) in localising deposition of new siliceous material. Based on our findings, we present a new model of diatom morphogenesis which is able to account for many morphological features of diatoms including the influence of environmental effects such as changes in pH and salinity, and the formation of a regular branched pattern.

Algorithms↗
PubMed1975

New concept of morphogenesis of clefts in the lip, alveolus, and palate.

The morphogenesis of clefts in the lip, alveolus, and palate is a process of both functional and formative adaptation of the affected mouth cavity to the disturbance which the cleft would represent in "pumping" the amniotic fluid. Only a normally developed portal venous system of the foetus, which is a continuation of the digestive canal through the liver, ensures efficient per-oral nutrition after birth. According to the findings known to date, the foetus feeds by "pumping" the amniotic fluid as early as the end of the third month of pregnancy. The amniotic fluid and nutritive substances contained in the fluid, which the foetus receives from the mother through the umbilical vein, are for the greatest part discharged through the foetus's skin. The morphogenesis of clefts proves the formative power of the tongue and its importance in the development of the mouth cavity as well as the ability of the normal growth response of the tissues around the cleft.

Alveolar Process↗