Basement membranes and cell movement.
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Animals↗
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Results for “Cell Movement”
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Serotonin, histamine, and norepinephrine mediation of endothelial and vascular smooth muscle cell movement.
The effects of serotonin (5-HT), histamine (H), and norepinephrine (NE) on bovine aortic endothelial cell (BAE) and vascular smooth muscle cell (VSM) movement were quantitated using a phagokinetic tracking assay. BAE movement was significantly reduced by 5-HT (31%), H (48%), and NE (62%) at concentrations ranging from 10(-10) to 10(-4) M (P less than 0.01). VSM motility was significantly enhanced by 5-HT (17%) and H (25%) at concentrations of 10(-8) and 10(-4)M, respectively (P less than 0.01). NE (10(-4)M) reduced VSM motility by 63% (P less than 0.01). Ketanserin (1 microM) reduced the 5-HT-associated inhibition of BAE movement by 75% (P less than 0.01). Diphenhydramine (1 microM) reduced the H-associated inhibition of BAE movement by 66% (P less than 0.01). Propranolol (1 microM) reduced NE-associated inhibition of BAE movement by 50% (P less than 0.01) and 5-HT-associated inhibition by 45% (P less than 0.05), but phenoxybenzamine had no significant effect. The results suggest 1) BAE and VSM are affected qualitatively in opposite ways by 5-HT and H; 2) the H-associated inhibition of BAE movement appears to be at least partially mediated by H1 receptors; 3) the 5-HT-associated inhibition of BAE movement may be mediated directly by a 5-HT binding component but indirectly by beta-adrenergic receptors; and 4) the NE-associated inhibition of BAE movement appears to be mediated by beta-adrenergic receptors.
Animals↗
Methanol exposure interferes with morphological cell movements in the Drosophila embryo and causes increased apoptosis in the CNS.
Despite the significant contributions of tissue culture and bacterial models to toxicology, whole animal models for developmental neurotoxins are limited in availability and ease of experimentation. Because Drosophila is a well understood model for embryonic development that is highly accessible, we asked whether it could be used to study methanol developmental neurotoxicity. In the presence of 4% methanol, approximately 35% of embryos die and methanol exposure leads to severe CNS defects in about half those embryos, where the longitudinal connectives are dorsally displaced and commissure formation is severely reduced. In addition, a range of morphological defects in other germ layers is seen, and cell movement is adversely affected by methanol exposure. Although we did not find any evidence to suggest that methanol exposure affects the capacity of neuroblasts to divide or induces inappropriate apoptosis in these cells, in the CNS of germ band retracted embryos, the number of apoptotic nuclei is significantly increased in methanol-exposed embryos in comparison to controls, particularly in and adjacent to the ventral midline. Apoptosis contributes significantly to methanol neurotoxicity because embryos lacking the cell death genes grim, hid, and reaper have milder CNS defects resulting from methanol exposure than wild-type embryos. Our data suggest that when neurons and glia are severely adversely affected by methanol exposure, the damaged cells are cleared by apoptosis, leading to embryonic death. Thus, the Drosophila embryo may prove useful in identifying and unraveling mechanistic aspects of developmental neurotoxicity, specifically in relation to methanol toxicity.
Animals↗
Transcellular cell movement and the formation of metastases.
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Animals↗
RNA helicase domain of tobamovirus replicase executes cell-to-cell movement possibly through collaboration with its nonconserved region.
UR-hel, a chimeric virus obtained by replacement of the RNA helicase domain of tobacco mosaic virus (TMV)-U1 replicase with that from the TMV-R strain, could replicate similarly to TMV-U1 in protoplasts but could not move from cell to cell (K. Hirashima and Y. Watanabe, J. Virol. 75:8831-8836, 2001). It was suggested that TMV recruited both the movement protein (MP) and replicase for cell-to-cell movement by unknown mechanisms. Here, we found that a recombinant, UR-hel/V, in which the nonconserved region was derived from TMV-R in addition to the RNA helicase domain of replicase, could move from cell to cell. We also analyzed revertants isolated from UR-hel, which recovered cell-to-cell movement by their own abilities. We found amino acid substitutions responsible for phenotypic reversion only in the nonconserved region and/or RNA helicase domain but never in MP. Together, these data show that both the nonconserved region and the RNA helicase domain of replicase are involved in cell-to-cell movement. The RNA helicase domain of tobamovirus replicase possibly does not interact directly with MP but interacts with its nonconserved region to execute cell-to-cell movement.
Plant Viral Movement Proteins↗
[Ultrastructural observation related to cell-to-cell movement and long-distance systemic transport on the hosts infected with BBWV 2].
The alteration of ultrastructure in Pisum sativum and Vicia faba leaf cells infected with B935 isolate of BBWV 2 were investigated by electron microscopy, immunogold-labeling technique. The results showed that the membranous proliferation, virus-formed crystals and tubular structures were found in leaf cells of two hosts. At early stages of infection, the tubules containing virus-like particles associate with plasmodesmata in mesophyll cell. Immunogold particles anti-BBWV 2 were localized to the plasmodesmata modified by tubules passing through them. The membranous proliferation and virus-formed tubules were also found in the parenchyma cells, companion cells and transfer cells of vascular bundle. Some virus-like particles located within sieve tube can be labeled immunogold particles anti-BBWV 2. These suggest that BBWV 2, similar CPMV, produce tubules extending into the plasmodesmata. Virions assembled in the cytoplasm are escorted to the tubular structures through interactions with their MP and are then transported to the adjacent cell. Many 160 nm in diameter virus-formed tubules in the cytoplasm, as a special aggregate, not directly relate to cell-to-cell movement; Intact virions are long-distance sustemic transported possibly through sieve elements.
Biological Transport↗
Pseudopodium dynamics and rapid cell movement in Dictyostelium Ras pathway mutants.
Loss of either of the Ras pathway members RasS or GefB causes growing Dictyostelium cells to move aberrantly rapidly. In this study, we describe the changes in motility that underlie these phenotypes using computer-assisted 3D dynamic image analysis. Unexpectedly, the two mutants use different mechanisms to achieve rapid migration. The rasS(-) cells' motility is characterised by highly dynamic cell morphology, with rapidly extending and retracting pseudopodia. The gefB(-) cells do not have an unusually dynamic morphology, and achieve their efficient translocation by the continual remodelling of an existing dominant anterior pseudopodium. In spite of these dramatic changes in pseudopodium behaviour, the underlying motility cycle of both mutants remains normal. The levels of F-actin in both mutant cell lines are significantly elevated with respect to the wild-type parental cells, suggesting a possible biochemical basis for these emphatic phenotypes.
Animals↗
A bipartite Tobacco mosaic virus-defective RNA (dRNA) system to study the role of the N-terminal methyl transferase domain in cell-to-cell movement of dRNAs.
Plant viruses, in particular Tobacco mosaic virus (TMV), are model systems to study RNA and protein trafficking in plants. Although TMV cell-to-cell transport controlled by the 30-kDa movement protein (MP) has been intensively studied, it was only recently demonstrated that the 126/183-kDa replicase proteins are also involved in cell-to-cell movement. Elucidating the role(s) of 126/183-kDa proteins in movement is complicated because these proteins have multiple functions associated with replication and gene expression. To overcome these difficulties we developed a TMV helper virus-defective RNA (dRNA) system to study the role of replicase protein sequences in dRNA cell-to-cell movement. Artificially constructed dRNAs lacking sequences encoding the helicase and polymerase domains of the replicase proteins and portions of the MP were viable in protoplasts and plants in the presence of helper virus. Expression of at least approximately 50% of the methyl transferase (MT) domain was required for efficient dRNA movement in Nicotiana benthamiana. dRNAs that encoded the N-terminal 64 replicase amino acids or lacked a translatable MT domain failed to move or moved poorly. TMV dRNAs expressing 258 amino acids of the replicase protein moved into all specialized non-vascular tissues, whereas dRNAs expressing replicase sequences beyond amino acid 258 were restricted to the epidermis and palisade mesophyll tissues. Furthermore, second-site mutations within the dRNA-encoded truncated replicase protein altered efficiency in dRNA cell-to-cell movement.
Base Sequence↗
Relationship between gene expression domains of Xsnail, Xslug, and Xtwist and cell movement in the prospective neural crest of Xenopus.
The markers Xslug, Xsnail, and Xtwist all are expressed in the presumptive neural folds and are thought to delineate the presumptive neural crest. However, their interrelationship and relative spatiotemporal distributions are not well understood. Here, we present a detailed in situ hybridization analysis of the relative patterns of expression of these transcription factors from gastrulation through neurulation and post-neural crest migration. The three genes mark the prospective neural crest and roof plate, coming on sequentially, with Xsnail preceding Xslug preceding Xtwist. By combining gene expression analysis with a fate map of the same region using DiI labeling, we determined the correspondence between early and late domains of gene expression. At the beginning of gastrulation, Xsnail is present in a unique domain of expression in a lateral region of the embryo in both superficial and deep layers of the ectoderm, as are Xslug and Xtwist. During gastrulation and neurulation, the superficial layer moves faster toward the dorsal midline than the deep layer, producing a relative shift in these cell populations. By early neurula stage, the Xsnail domain is split into a medial domain in the superficial ectoderm (fated to become the roof plate) and a lateral domain in the deep layer of the ectoderm (fated to become neural crest). Xsnail is down-regulated in the most anterior neural plate and up-regulated in the posterior neural plate. Our results show that changes in the expression of Xsnail, Xslug, and Xtwist are a consequence of active cell movement in some regions coupled with dynamic changes in gene expression in other regions.
Animals↗
HSP70 homolog functions in cell-to-cell movement of a plant virus.
Plant closteroviruses encode a homolog of the HSP70 (heat shock protein, 70 kDa) family of cellular proteins. To facilitate studies of the function of HSP70 homolog (HSP70h) in viral infection, the beet yellows closterovirus (BYV) was modified to express green fluorescent protein. This tagged virus was competent in cell-to-cell movement, producing multicellular infection foci similar to those formed by the wild-type BYV. Inactivation of the HSP70h gene by replacement of the start codon or by deletion of 493 codons resulted in complete arrest of BYV translocation from cell to cell. Identical movement-deficient phenotypes were observed in BYV variants possessing HSP70h that lacked the computer-predicted ATPase domain or the C-terminal domain, or that harbored point mutations in the putative catalytic site of the ATPase. These results demonstrate that the virus-specific member of the HSP70 family of molecular chaperones functions in intercellular translocation and represents an additional type of a plant viral-movement protein.
Adenosine Triphosphatases↗
A new model for the quantitative analysis of cell movements in vitro: definition of a shape change factor.
Changes in shape, in addition to translocations, are an important aspect of cell motility. We propose a simple geometrical model for the quantitative analysis of shape changes undergone by cultured cells. The extent to which images of a given cell do not overlap at the beginning and end of a time interval is used as a measure of motility, and a translation step included to eliminate translocation effects. Initial findings suggest that the method is widely applicable.
Animals↗
Convergent extension: the molecular control of polarized cell movement during embryonic development.
During development, vertebrate embryos undergo dramatic changes in shape. The lengthening and narrowing of a field of cells, termed convergent extension, contributes to a variety of morphogenetic processes. Focusing on frogs and fish, we review the different cellular mechanisms and the well-conserved signaling pathways that underlie this process.
Animals↗
Conserved patterns of cell movements during vertebrate gastrulation.
Vertebrate embryogenesis entails an exquisitely coordinated combination of cell proliferation, fate specification and movement. After induction of the germ layers, the blastula is transformed by gastrulation movements into a multilayered embryo with head, trunk and tail rudiments. Gastrulation is heralded by formation of a blastopore, an opening in the blastula. The axial side of the blastopore is marked by the organizer, a signaling center that patterns the germ layers and regulates gastrulation movements. During internalization, endoderm and mesoderm cells move via the blastopore beneath the ectoderm. Epiboly movements expand and thin the nascent germ layers. Convergence movements narrow the germ layers from lateral to medial while extension movements elongate them from head to tail. Despite different morphology, parallels emerge with respect to the cellular and genetic mechanisms of gastrulation in different vertebrate groups. Patterns of gastrulation cell movements relative to the blastopore and the organizer are similar from fish to mammals, and conserved molecular pathways mediate gastrulation movements.
Animals↗
A link between cell movement and gene expression argues that motility is required for cell-cell signaling during fruiting body development.
Nonmotile mutants of Myxococcus xanthus (Myxobacterales) failed to execute the morphogenetic movements required to shape a fruiting body. In addition, nonmotile mutants produced very few spores when plated for fruiting body development at cell densities appropriate for wild-type cells. At higher initial cell densities, the proportion of nonmotile cells that sporulate increased, indicating that one important function of motility in fruiting body development is to increase the local cell density. However, even at 10 times normal cell density, nonmotile cells sporulated at only 1% the wild-type level. This sporulation deficiency of nonmotile mutants accompanies an altered pattern of gene expression, monitored by using transcriptional fusions of lacZ to genes expressed at specific times during fruiting body development. Motility was not required for normal expression of five lac fusions that are expressed within the first 6 hr of fruiting-body development. However, the levels of expression from five lac fusions to later-expressed genes were reduced or abolished in nonmotile strains. beta-Galactosidase expression in these late Tn5 lac insertions was increased, and fruiting body development occurred in certain nonmotile strains that can be stimulated to move when mixed with a donor strain. This shows that motility itself is required because the stimulated cells are nonmotile genotypically. The nonmotile mutations had the same effect on developmental beta-galactosidase expression from these 10 lac fusions as an insertion mutation in the csg (formerly spoC) gene. csg mutants have a cell-cell interaction defect that blocks fruiting body development at approximately 6 hr. The similarity in the pattern of developmental expression of motility mutants and csg mutants suggests that motility is required for this csg-mediated cell-cell interaction.
Cell Movement↗
New insights into galvanotaxis and other directed cell movements: an analysis of the translocation distribution function.
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Animals↗
Cell-to-cell movement of beet necrotic yellow vein virus: I. Heterologous complementation experiments provide evidence for specific interactions among the triple gene block proteins.
Cell-to-cell movement of beet necrotic yellow vein virus (BNYVV) requires three proteins encoded by a triple gene block (TGB) on viral RNA 2. A BNYVV RNA 3-derived replicon was used to express movement proteins to functionally substitute for the BNYVV TGB proteins was tested by coinoculation of TGB-defective BNYVV with the various replicons to Chenopodium quinoa. Trans-heterocomplementation was successful with the movement protein (P30) of tobacco mosaic virus but not with the tubule-forming movement proteins of alfalfa mosaic virus and grapevine fanleaf virus. Trans-complementation of BNYVV movement was also observed when all three TGB proteins of the distantly related peanut clump virus were supplied together but not when they were substituted for their BNYVV counterparts one by one. When P30 was used to drive BNYVV movement in trans, accumulation of the first TGB protein of BNYVV was adversely affected by null mutations in the second and third TGB proteins. Taken together, these results suggest that highly specific interactions among cognate TGB proteins are important for their function and/or stability in planta.
Genes, Viral↗
Cell-to-cell movement of the 25K protein of potato virus X is regulated by three other viral proteins.
The 25K, 12K, and 8K proteins and coat protein (CP) of Potato virus X (PVX) are required for virus cell-to-cell movement. In this study, experiments were conducted to determine whether the PVX 25K protein moves cell to cell and to explore potential interactions between the PVX 25K, 12K, and 8K proteins and CP. The PVX 25K gene was fused to the green fluorescent protein (GFP) gene and inserted into plasmids adjacent to the cauliflower mosaic virus 35S promoter. These plasmids were introduced by biolistic bombardment to transgenic tobacco expressing the PVX 12K, 8K, and CP genes. The GFP:25K fused proteins moved cell to cell on nontransgenic tobacco and tobacco expressing either the 12K or 8K proteins. However, the GFP:25K proteins did not move on transgenic tobacco expressing the combined 12K/8K genes or the CP gene. Thus, movement of the PVX 25K protein through plasmodesmata may be regulated by interactions with other PVX proteins.
Biological Transport↗
Cell movement during chick primitive streak formation.
Gastrulation in amniotes begins with extensive re-arrangements of cells in the epiblast resulting in the formation of the primitive streak. We have developed a transfection method that enables us to transfect randomly distributed epiblast cells in the Stage XI-XIII chick blastoderms with GFP fusion proteins. This allows us to use time-lapse microscopy for detailed analysis of the movements and proliferation of epiblast cells during streak formation. Cells in the posterior two thirds of the embryo move in two striking counter-rotating flows that meet at the site of streak formation at the posterior end of the embryo. Cells divide during this rotational movement with a cell cycle time of 6-7 h. Daughter cells remain together, forming small clusters and as result of the flow patterns line up in the streak. Expression of the cyclin-dependent kinase inhibitor, P21/Waf inhibits cell division and severely limits embryo growth, but does not inhibit streak formation or associated flows. To investigate the role off cell-cell intercalation in streak formation we have inhibited the Wnt planar-polarity signalling pathway by expression of a dominant negative Wnt11 and a Dishevelled mutant Xdd1. Both treatments do not result in an inhibition of streak formation, but both severely affect extension of the embryo in later development. Likewise inhibition of myosin II which as been shown to drive cell-cell intercalation during Drosophila germ band extension, has no effect on streak formation, but also effectively blocks elongation after regression has started. These experiments make it unlikely that streak formation involves known cell-cell intercalation mechanisms. Expression of a dominant negative FGFR1c receptor construct as well as the soluble extracellular domain of the FGFR1c receptor both effectively block the cell movements associated with streak formation and mesoderm differentiation, showing the importance of FGF signalling in these processes.
Animals↗