[Adenosinetriphosphate as the energy substance for cell movement].
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Adenosine Triphosphate↗
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Results for “Cell Movement”
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Multiple serine phosphorylation sites on the 30 kDa TMV cell-to-cell movement protein synthesized in tobacco protoplasts.
p30, the protein required for cell-to-cell movement of tobacco mosaic virus (TMV), has a slightly reduced mobility on SDS-polyacrylamide gels when isolated by immunoprecipitation from TMV-infected protoplasts compared with that of p30 translated from viral RNA in vitro. Further investigation established a probable cause for the difference in mobility between the two: protoplasts incorporate [32P]orthophosphate into p30 at multiple sites, predominantly as phosphoserine. Tryptic peptide mapping reveals at least five internal phosphopeptides in p30, besides the C-terminal tryptic phosphopeptide already reported, involving at least two distinct domains of the protein (at residues 61-114 and residues 212-231), which may be substrates for different protein kinases. These structural results are consistent with a three-domain model for the TMV movement protein with two regulatory domains similar to that recently proposed on genetic grounds for dianthovirus movement proteins.
Peptide Mapping↗
Letters to the editor: Is the upper cell surface unable to support active cell movement in culture?
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Animals↗
[Interrelation between cell surface and cell movement: importance for tumor penetration].
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Cell Membrane↗
Electrical phenomena associated with cell movements.
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Cell Biology↗
The potato virus X TGBp2 protein association with the endoplasmic reticulum plays a role in but is not sufficient for viral cell-to-cell movement.
Potato virus X (PVX) TGBp1, TGBp2, TGBp3, and coat protein are required for virus cell-to-cell movement. Plasmids expressing GFP fused to TGBp2 were bombarded to leaf epidermal cells and GFP:TGBp2 moved cell to cell in Nicotiana benthamiana leaves but not in Nicotiana tabacum leaves. GFP:TGBp2 movement was observed in TGBp1-transgenic N. tabacum, indicating that TGBp2 requires TGBp1 to promote its movement in N. tabacum. In this study, GFP:TGBp2 was detected in a polygonal pattern that resembles the endoplasmic reticulum (ER) network. Amino acid sequence analysis revealed TGBp2 has two putative transmembrane domains. Two mutations separately introduced into the coding sequences encompassing the putative transmembrane domains within the GFP:TGBp2 plasmids and PVX genome, disrupted membrane binding of GFP:TGBp2, inhibited GFP:TGBp2 movement in N. benthamiana and TGBp1-expressing N. tabacum, and inhibited PVX movement. A third mutation, lying outside the transmembrane domains, had no effect on GFP:TGBp2 ER association or movement in N. benthamiana but inhibited GFP:TGBp2 movement in TGBp1-expressing N. tabacum and PVX movement in either Nicotiana species. Thus, ER association of TGBp2 may be required but not be sufficient for virus movement. TGBp2 likely provides an activity for PVX movement beyond ER association.
Amino Acid Sequence↗
Extensive cell movements accompany formation of the otic placode.
During development, the vertebrate inner ear arises from the otic placode, a thickened portion of the ectoderm next to the hindbrain. Here, the first detailed fate maps of this region in the chick embryo are presented. At head process stages, placode precursors are scattered throughout a large region of the embryonic ectoderm, where they intermingle with future neural, neural crest, epidermal, and other placode cells. Within the next few hours, dramatic cell movements shift the future otic placode cells toward the midline and ultimately result in convergence to their final position next to rhombomeres 5-6. Individual cells and small cell groups undergo constant cell rearrangements and appear to sort out from nonotic cells. While the major portion of the otic placode is derived from the nonneural ectoderm, the neural folds also contribute cells to the placode at least until the four-somite stage. Comparison of these fate maps with gene expression patterns at equivalent stages reveals molecular heterogeneity of otic precursor cells in terms of their expression of dlx5, msx1, Six4, and ERNI. Although Pax2 expression coincides with the region where otic precursors are found from stage 8, not all Pax2-positive cells will ultimately contribute to the otic placode.
Animals↗
A coordinated change in chemokine responsiveness guides plasma cell movements.
Antibody-secreting plasma cells are nonrecirculatory and lodge in splenic red pulp, lymph node medullary cords, and bone marrow. The factors that regulate plasma cell localization are poorly defined. Here we demonstrate that, compared with their B cell precursors, plasma cells exhibit increased chemotactic sensitivity to the CXCR4 ligand CXCL12. At the same time, they downregulate CXCR5 and CCR7 and have reduced responsiveness to the B and T zone chemokines CXCL13, CCL19, and CCL21. We demonstrate that CXCL12 is expressed within splenic red pulp and lymph node medullary cords as well as in bone marrow. In chimeric mice reconstituted with CXCR4-deficient fetal liver cells, plasma cells are mislocalized in the spleen, found in elevated numbers in blood, and fail to accumulate normally in the bone marrow. Our findings indicate that as B cells differentiate into plasma cells they undergo a coordinated change in chemokine responsiveness that regulates their movements in secondary lymphoid organs and promotes lodgment within the bone marrow.
Animals↗
Embryonic development of the rat cerebellum. I. Delineation of the cerebellar primordium and early cell movements.
Short-survival and long-survival thymidine radiograms, and methacrylate-embedded tissue from normal and X-irradiated rat embryos were used to delineate the neuroepithelial source of the cerebellum and trace the earliest cell movements. The cerebellar anlage, crescent shaped, is demarcated by two ventricular landmarks, the anterior extension of the tela choroidea of the fourth ventricle and the embryonic cerebellar fissure. The cerebellar tela choroidea extends from the medullary fourth ventricle posteromedially to the lateral recess of the pontine fourth ventricle anterolaterally. The embryonic cerebellar fissure begins caudally as a single midline incision beneath the fused posterior cerebellar primordium, then splits to follow the unfused cerebellar halves, first separating each from the isthmus then from the pons. The cerebellar primordium is divided into three parts. The lateral cerebellar primordium caps the lateral recess of the fourth ventricle; it is contiguous with the pons medially and separated ventrally from the anlage of the cochlear nuclei by the tela choroidea. The subisthmal cerebellar primordium is situated beneath the isthmus, medially lining the isthmus canal. Laterally and posteriorly, it is continuous with the lateral and postisthmal primordia. The postisthmal cerebellar primordium caps the postisthmal recess of the fourth ventricle and extends to the medullary fourth ventricle. As we shall describe later, each of these primordia is a source of different components of the developing cerebellum. Most cells of the superficially located nuclear transitory zone are labeled with 3H-thymidine administered on day E14 but not thereafter. A high proportion of the cells of the deeper cortical transitory zone could still be labeled on day E15. This supports the assumption made earlier that the first is composed of differentiating deep neurons, the second of Purkinje cells. The cells of the nuclear transitory zone originate in the lateral cerebellar primordium near the junction with the tela choroidea prior to the formation of the germinal trigone and migrate in a superficial position medially. Beginning on day E16, the nuclear transitory zone splits into two components. One has transversely oriented cells that seem to be the source of a decussating fiber tract, presumably the hook bundle of Russell. The other is composed of longitudinally oriented cells that apparently contribute fibers to the ipsilateral superior cerebellar peduncle. The translocation of the cells of the nuclear transitory zone from the cerebellar surface to its depth, to form the deep nuclei, and the radial migration of the cells of the cortical transitory zone to the surfa
Animals↗
Generation of splenic follicular structure and B cell movement in tumor necrosis factor-deficient mice.
Secondary lymphoid tissue organogenesis requires tumor necrosis factor (TNF) and lymphotoxin alpha (LTalpha). The role of TNF in B cell positioning and formation of follicular structure was studied by comparing the location of newly produced naive recirculating and antigen-stimulated B cells in TNF-/- and TNF/LTalpha-/- mice. By creating radiation bone marrow chimeras from wild-type and TNF-/- mice, formation of normal splenic B cell follicles was shown to depend on TNF production by radiation-sensitive cells of hemopoietic origin. Reciprocal adoptive transfers of mature B cells between wild-type and knockout mice indicated that normal follicular tropism of recirculating naive B cells occurs independently of TNF derived from the recipient spleen. Moreover, soluble TNF receptor-IgG fusion protein administered in vivo failed to prevent B cell localization to the follicle or the germinal center reaction. Normal T zone tropism was observed when antigen-stimulated B cells were transferred into TNF-/- recipients, but not into TNF/LTalpha-/- recipients. This result appeared to account for the defect in isotype switching observed in intact TNF/LTalpha-/- mice because TNF/LTalpha-/- B cells, when stimulated in vitro, switched isotypes normally. Thus, TNF is necessary for creating the permissive environment for B cell movement and function, but is not itself responsible for these processes.
Animals↗
Cell movement elicited by epidermal growth factor receptor requires kinase and autophosphorylation but is separable from mitogenesis.
The EGF receptor (EGFR) upon activation signals increased cell movement. However, the domains within the receptor, and the pathway which trigger movement are undefined. We expressed EGFR mutants at physiologic levels in receptor-devoid NR6 cells to investigate this biologic response. The receptors possessed kinase activity and underwent autophosphorylation as predicted by primary amino acid sequence. EGF-induced cell motility was assessed in vitro by excess migration into an acellular area and colony scatter in the presence of saturating concentrations of EGF. Wild-type (WT)-EGFR signaled increased motility. However, replacing the conserved lysine721 with methionine resulted in a kinase-inactive receptor which did not elicit movement. Removal of the entire terminus by truncation (c'973) also abrogated ligand-induced motility. Thus, we concentrated on the carboxy-terminal domains. EGF-induced movement was seen with a less-truncated mutant (c'1000) that contained a single autophosphorylated tyrosine (tyrosine992). Other mutants, c'991 and c'1000F992, in which this tyrosine was removed did not signal motility. Fusion mutants which presented other autophosphorylated tyrosine domains also exhibited EGF-induced movement. These findings suggested that the presence of both an autophosphorylated tyrosine signaling domain and the kinase activity are necessary for this biologic response. All kinase-positive mutants signaled cell proliferation but only those that contained autophosphorylatable tyrosines induced movement. The motility responses mediated by these EGFR were identical in the presence or absence of mitomycin-C, at a dose (0.5 micrograms/ml) which completely inhibited cell proliferation. On the other side, D-actinomycin (50 ng/ml) blocked EGF-induced motility but did not affect thymidine incorporation. Thus, EGF-induced mitogenesis and cell motility are mediated through different pathways.
Amino Acid Sequence↗
Cinemicrographic study of the cell movement in the primitive-streak-stage mouse embryo.
Migration of the mesoderm cells in the primitive-streak-stage mouse embryo was directly studied by cinemicrography using whole embryo culture and Nomarski differential interference contrast optics. Relative transparency and small size of the early mouse embryos enabled direct observation of the individual cells and their cell processes. Seven-day-old mouse embryos were isolated and cultured in a small chamber in a medium consisting of 50% rat serum and 50% Dulbecco's modified minimum essential medium. The mesoderm cells move away from the primitive streak in both anterior and antimesometrial (distal) directions at a mean velocity of 46 micron h-1. They extend cell processes and constantly change cell shape. They do not translocate extensively as isolated single cells, but usually maintain attachment to other mesoderm cells. They show frequent cell division preceded by rounding up of the cell bodies, and accompanied by vigorous blebbing before and after cytokinesis. This study shows that it is possible to examine the motility of embryonic cells inside the mammalian embryo by direct observation if the embryo is small and transparent enough for the use of the Nomarski optics.
Animals↗
Cell movements during vertebrate development: integrated tissue behaviour versus individual cell migration.
Cell migration during development is fundamental to the establishment of the embryonic architecture. Depending on the context, cells may move either as integrated sheets of tissue or individually. Recently, molecules that are involved in both these types of cell behaviour have been identified, helping us to understand developmental processes as important as gastrulation and neural crest formation, and ultimately, the morphogenetic movements that shape the embryo.
Animals↗
Responses to Wnt signals in vertebrate embryos may involve changes in cell adhesion and cell movement.
Wnt genes encode secreted glycoproteins, and, because of their homology with the Drosophila segment polarity gene wingless, are likely to play important roles as modulators of local intercellular signalling during embryonic development. Although little is known of the mechanisms by which Wnts signal in an autocrine or paracrine manner, it is increasingly clear that cells can respond rapidly to Wnt signals in the absence of transcription, and that these responses may include changes in cell adhesion and cell movement. We review recent evidence from studies on Xenopus laevis and other systems, which demonstrate that (1) a subset of Wnts modulate gap junctional permeability, which may be a reflection of changes in cadherin-mediated cell adhesion, (2) embryos express beta-catenin and plakoglobin, which are homologs of the armadillo gene products, known to be involved in the wingless signalling pathway, and known to be found at cell junctions, and (3) overexpression of specific Wnts in Xenopus embryos leads to clear changes in cell behavior and movement.
Animals↗
Cell movement and contraction in somite development.
During somite formation the segmental plate mesoderm, lying on either side of the axial organs, reorganizes into roughly spherical pairs of epithelial structures. This segmentation process includes changes in cell shape and position, cell-cell and cell-substratum adhesive properties and accumulation of extracellular matrix material which proceed down the anterior-posterior axis. Later in somite development the sclerotome region "disperses", migrating around the spinal cord where it produces the cartilage model of the vertebral column. Experimental manipulation of segmentation and sclerotome dispersal with drugs affecting microfilaments, microtubules and calcium-dependent contraction suggest that cells migrate into position, elongate, and undergo apical contraction as part of the segmentation process. This process of calcium-dependent, possibly calmodulin-mediated, contraction can be both stimulated precociously and inhibited, showing similarities with contractile morphogenetic events in epithelial organ systems such as eye and thyroid. Similar experiments with drugs affecting contractile microfilaments demonstrate that active cell movement, along with extracellular matrix production, is involved in sclerotome dispersal.
Animals↗
From a discrete to a continuous model of biological cell movement.
The process by which one may take a discrete model of a biophysical process and construct a continuous model based upon it is of mathematical interest as well as being of practical use. In this work, we take the extended Potts model applied to biological cell movement to its continuous limit. Beginning with a single cell moving in one dimension on a lattice and obeying Potts model rules of movement we develop an expression for the diffusion coefficient of a collection of noninteracting cells which depends explicitly on the Potts model parameters. We show how this coefficient varies when the Potts parameters for cell membrane elasticity and cell-medium adhesion are varied, and perform computer simulations which support our theoretical result. We explain the relationship between the probability of occupancy of lattice points and the density profile in the continuous limit, and extend our analysis by including interactions between the cells. In so doing we are able to develop a set of coupled ordinary differential equations showing the evolution of a density profile in the presence of significant cell-cell adhesion, and show how increases in the strength of this adhesion modulates diffusion. In so doing we develop some insights into how continuous models of physical systems can be based upon discrete models which describe the same system.
Animals↗
A quantitative assay to study cell movement in the myxobacteria.
A simple quantitative assay has been developed to test the rate of cell movement of myxobacteria. The assay employs an agar surface and at no time are the cells cultured in a liquid environment. Isolation of a rate-increasing substance(s) from fruiting Myxococcus xanthus is reported. The understanding of the aggregative process in these bacteria will be aided by characterization of the chemotactic system.
Agar↗
Stat3 Controls Cell Movements during Zebrafish Gastrulation.
Vertebrate axis formation requires both the correct specification of cell fates and the coordination of gastrulation movements. We report that the zebrafish signal transducer and activator of transcription 3 (Stat3) is activated on the dorsal side by the maternal Wnt/beta-catenin pathway. Zebrafish embryos lacking Stat3 activity display abnormal cell movements during gastrulation, resulting in a mispositioned head and a shortened anterior-posterior axis, but show no defects in early cell fate specification. Time course analysis, cell tracing, and transplantation experiments revealed that Stat3 activity is required cell autonomously for the anterior migration of dorsal mesendodermal cells and non-cell autonomously for the convergence of neighboring paraxial cells. These results reveal a role for Stat3 in controlling cell movements during gastrulation.
Animals↗