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PubMed1974

The upper cell surface: its inability to support active cell movement in culture.

A variety of epithelial cells and fibroblasts fail to move over one another's upper surfaces in culture, resulting in monolayering. The failure of seeded fibroblasts to adhere to and spread on epithelial cell surfaces suggests that monolayering in culture is due to the lack of adhesion of the upper cell surface, at least of epithelial cells. Seeded fibroblasts and postmitotic, rounded fibroblasts likewise fail to spread on the upper surfaces of spread fibroblasts, suggesting that the inability of the upper cell surface to support spreading may be a general phenomenon. Inert particles and cell processes do not adhere directly to the upper cell surface. However, they can initiate adhesions to the surface at a cell's free margin, suggesting a variation of adhesive properties over a cell's surface.

Animals↗
PubMed2002

Cell movements during gastrulation: snail dependent and independent pathways.

The morphogenetic process of gastrulation requires multiple inputs and intricate coordination. Genetic analyses demonstrate critical roles of vertebrate and invertebrate Snail proteins in this process. Together with other regulatory molecules including Wnt and BMP, the Snail pathways specify cell fate and reorganize cellular machineries to coordinate morphological changes and cell movements during gastrulation.

Adherens Junctions↗
PubMed1998

Tumour cell movement during heating and humidification of insufflating CO2: an in vitro model.

BACKGROUND: Intra-operative hypothermia and port-site recurrence have been associated with laparoscopic surgery. Heating and humidification of insufflating CO2 may protect against laparoscopy-associated hypothermia. However, the effect of heated, humidified CO2 upon tumour cell movement is unknown. METHODS: Twenty-four in vitro studies that used 4-L plastic bottles were performed. Thirteen million human colorectal cancer cells were placed in each bottle. Twelve studies used dry room temperature CO2 for insufflation: the remaining 12 used heated, humidified CO2 as the insufflating gas. Both groups were subdivided into bottles with leaks around the trocars and with airtight sealing around the trocars. Two trocars and a laparoscopic grasper were used. The exiting insufflating gas was filtered and examined for the presence of cells. Laparoscopic instruments agitated the contents of the bottles. The instruments and trocars were washed. These washings were examined for the presence of cells. RESULTS: Heated, humidified CO2 insufflation was able to maintain a warmer and more humid environment within the bottles when compared with dry room-temperature CO2. No cells were detected on the gas filters. Tumour cells were found on 12 out of 12 instruments and 11 out of 12 trocars with dry CO2 insufflation. Tumour cells were found on 8 out of 12 instruments and 7 out of 12 trocars with heated humidified CO2 insufflation. The only statistically significant difference in tumour cell spread to trocars was found between heating and humidification when no leak was present, and heating and humidification with leak present, and dry insufflation with no leak present (P = 0.015, Fisher's two-tailed exact test). CONCLUSIONS: Heating and humidifying CO2 during in vitro laparoscopy does not increase the aerosolization of tumour cells when compared with dry CO2. However, the use of heated and humidified gas with airtight seals around the trocars in vitro may lessen cell deposition on trocars.

Carbon Dioxide↗
PubMed1997

The tracheae defective gene encodes a bZIP protein that controls tracheal cell movement during Drosophila embryogenesis.

The tracheae defective (tdf) gene is required for the formation of the tracheal system during Drosophila embryogenesis. It encodes a putative bZIP transcription factor (TDF). Antibodies directed against TDF detect a nuclear protein in all tracheal cells before invagination and throughout tracheal system morphogenesis. Examination of tdf mutants revealed that tdf activity is not necessary for determining tracheal cell identity but for subsequent morphogenetic cell movements. tdf activity is under the control of trachealess, the key regulator gene for tracheal development. In contrast, tdf activity is not dependent on and does not interfere with the fibroblast growth factor- (FGF) and Decapentaplegic- (DPP) mediated signalling that direct guided tracheal cell migration. Our results suggest that lack of tdf activity affects tracheal cell migration in general rather than specific aspects of cell migration. tdf activity involves a maternal and zygotic component and its requirement is not limited to tracheal system formation. The complex spatiotemporal patterns of TDF expression in the embryo correspond to defects, suggesting that cell migration is impaired. We propose that the bZIP protein TDF functions as a co-regulator of target genes that provide cells with the ability to migrate.

Amino Acid Sequence↗
PubMed1998

Unconventional myosins in cell movement, membrane traffic, and signal transduction.

In the past few years genetic, biochemical, and cytolocalization data have implicated members of the myosin superfamily of actin-based molecular motors in a variety of cellular functions including membrane trafficking, cell movements, and signal transduction. The importance of myosins is illustrated by the identification of myosin genes as targets for disease-causing mutations. The task at hand is to decipher how the multitude of myosins function at both the molecular and cellular level-a task facilitated by our understanding of myosin structure and function in muscle.

Animals↗
PubMed2000

Focal adhesion kinase: a regulator of focal adhesion dynamics and cell movement.

Engagement of integrin receptors with extracellular ligands gives rise to the formation of complex multiprotein structures that link the ECM to the cytoplasmic actin cytoskeleton. These adhesive complexes are dynamic, often heterogeneous structures, varying in size and organization. In motile cells, sites of adhesion within filopodia and lamellipodia are relatively small and transient and are referred to as 'focal complexes,' whereas adhesions underlying the body of the cell and localized to the ends of actin stress fibers are referred to as 'focal adhesions'. Signal transduction through focal complexes and focal adhesions has been implicated in the regulation of a number of key cellular processes, including growth factor induced mitogenic signals, cell survival and cell locomotion. The formation and remodeling of focal contacts is a dynamic process under the regulation of protein tyrosine kinases and small GTPases of the Rho family. In this review, we consider the role of the focal complex associated protein tyrosine kinase, Focal Adhesion Kinase (FAK), in the regulation of cell movement with the emphasis on how FAK regulates the flow of signals from the ECM to the actin cytoskeleton.

Actins↗
PubMed1983

A rat monoclonal antibody reacting specifically with the tyrosylated form of alpha-tubulin. II. Effects on cell movement, organization of microtubules, and intermediate filaments, and arrangement of Golgi elements.

A rat monoclonal antibody against yeast alpha-tubulin (clone YL 1/2; Kilmartin, J. V., B. Wright, and C. Milstein, 1982, J. Cell Biol., 93:576-582) that reacts specifically with the tyrosylated form of alpha-tubulin and readily binds to tubulin in microtubules when injected into cultured cells (see Wehland, J., M. C. Willingham, and I. V. Sandoval, 1983, J. Cell Biol., 97:1467-1475) was used to study microtubule organization and function in living cells. Depending on the concentration of YL 1/2 that was injected the following striking effects were observed: (a) When injected at a low concentration (2 mg IgG/ml in the injection solution), where microtubules were decorated without changing their distribution, intracellular movement of cell organelles (saltatory movement) and cell translocation were not affected. Intermediate concentrations (6 mg IgG/ml) that induced bundling but no perinuclear aggregation of microtubules abolished saltatory movement and cell translocation, and high concentrations (greater than 12 mg IgG/ml) that induced perinuclear aggregation of microtubules showed the same effect. (b) YL 1/2, when injected at intermediate and high concentrations, arrested cells in mitosis. Such cells showed no normal spindle structures. (c) Injection of an intermediate concentration of YL 1/2 that stopped saltatory movement caused little or no aggregation of intermediate filaments and no dispersion of the Golgi complex. After injection of high concentrations, resulting in perinuclear aggregation of microtubules, intermediate filaments formed perinuclear bundles and the Golgi complex became dispersed analogous to results obtained after treatment of cells with colcemid. (d) When rhodamine-conjugated YL 1/2 was injected at concentrations that stopped saltatory movement and arrested cells in mitosis, microtubule structures could be visualized and followed for several hours in living cells by video image intensification microscopy. They showed little or no change in distribution and organization during observation, even though these microtubule structures appeared not to be stabilized by injected YL 1/2 since they were readily depolymerized by colcemid or cold treatment and repolymerized upon drug removal or rewarming to 37 degrees C, respectively. These results are discussed in terms of the participation of microtubules in cellular activities such as cell movement and cytoplasmic organization and in terms of the specificity of YL 1/2 for the tyrosylated form of alpha-tubulin.

Animals↗
PubMed1995

Cell-to-cell movement of potato virus X revealed by micro-injection of a viral vector tagged with the beta-glucuronidase gene.

The replication and cell-to-cell movement of potato virus X (PVX) has been studied using a PVX vector construct which expressed the beta-glucuronidase (GUS) reporter gene in infected cells. Nicotiana clevelandii leaf trichome cells were micro-injected with the PVX-GUS vector and histochemical staining was used to locate GUS activity. The distribution of GUS activity revealed that PVX had moved from the injected cell into other trichome cells and into the cells along the leaf margin. GUS activity was always restricted to the cells at the edge of the leaf suggesting that PVX was unable to move out of the marginal cells. At the infection front, scattered along the leaf margin, there were isolated groups of cells staining for GUS activity. The absence of GUS activity in the intervening cells suggests that PVX had moved through several cells without replicating within them. This latter observation is consistent with previously reported observations that viral movement proteins are capable of moving between cells.

Genetic Vectors↗
PubMed2003

Conserved requirement of Lim1 function for cell movements during gastrulation.

To investigate Lim1 function during gastrulation, we used transcript depletion through DEED antisense oligonucleotides in Xenopus and cell transplantation in mice. Xenopus embryos depleted of Lim1 lack anterior head structures and fail to form a proper axis as a result of a failure of gastrulation movements, even though mesodermal cell identities are specified. Similar disruption of cell movements in the mesoderm is also observed in Lim1(-/-) mice. Paraxial protocadherin (PAPC) expression is lost in the nascent mesoderm of Lim1(-/-) mouse embryos and in the organizer of Lim1-depleted Xenopus embryos; the latter can be rescued to a considerable extent by supplying PAPC exogenously. We conclude that a primary function of Lim1 in the early embryo is to enable proper cell movements during gastrulation.

Animals↗
PubMed1965

CELL MOVEMENTS.

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Cell Movement↗