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At least 163 records · Page 9Linked to original sources
PubMed1975

XC-cell fusion induced by murine plasmocytoma cells. II. Cytological and ultrastructural study.

The MF2 strain, a mouse myeloma derived cell line, was found to induce the mixed culture cytopathogenicity test when cocultured with XC cells. Only one MF2 cell was present per syncytium, as shown by autoradiography. Pretreatment of cells with inhibitors of DNA, RNA or protein synthesis suggested that a normal RNA synthesis was required to obtain optimal polykaryon growth. Immunoelectron microscopy using a syngenic mouse MF2 cell antiserum and peroxydase labeling revealed a complete mixing and redistribution of the respective plasma membrane sites of MF2 and XC cells on polykaryon surface.

Animals↗
PubMed1976

XC-cell fusion induced by murine plasmocytoma cell. III. RNA gene expression correlated to syncytium formation.

The MF2 strain, a mouse myeloma derived cell line, was found to continuously produce C-type viral particles when maintained in tissue-culture. These cells when cultured in an ascitic form by injection to Balb/c mice lost this property. The ability to induce syncytia by cocultivation of the MF2 cell with XC-cells was shown to be related to the viral production. A DNA complementary to viral 70 S RNA was synthesized using the viral reverse-transcriptase endogenous activity. The quality of the probe is discussed and the expression of the viral genome among cellular poly A rich RNA varied concomitently to the syncytium inducing ability as evidenced by molecular hybridization experiments.

Animals↗
PubMed1990

[Induced cell fusion in the contact zone of cells with affected and unaffected surfaces. I].

The change in capacity of the cell fusion stimulated with polyethylenglycol is applied as a criterion of accumulation of noxiously transformed properties of cell surfaces. Similar changes are induced with substances employed as follows: chinuclidyl benzilate, atropiniumsulphate, tetrahydroaminacridine. The dynamics of releasing these substances is also tracked by dynamics of fusions capacity. In the area of contact of cells both noxiously influenced and uninfluenced, the decrease in capacity of fusions is also observed. At least a part of toxical substance is so released outside the cells. The former is then linked to the surfaces of unfluenced cells. This is an example of transfer of substance linked with the cell surface which is concerned.

Atropine↗
PubMed1983

Macrocyst development in Dictyostelium discoideum. III. Cell-fusion inducing factor secreted by giant cells.

A factor was discovered that markedly enhances the degree of fusion activity between cells of the opposite mating-type strains, MI1 and NC4, in the sexual cycle of Dictyostelium discoideum. This factor, designated cell-fusion inducing factor (CFIF), was detected initially in supernatants taken from 24 h dark-grown mixed cultures of HM1 and NC4 cells, and subsequently shown to be secreted by giant cells - the fusion products of HM1 and NC4 cells. HM1 cells, cultured in the dark at appropriate temperature, normally acquire fusion-competence specific to NC4 cells. The addition of CFIF to such dark-grown HM1 cultures results in a marked increase in their fusion-competence. In addition, when CFIF is added to light-grown HM1 cultures, in which cells normally do not acquire the ability to fuse with NC4 cells, fusion-competence is induced. The fusion-competence of NC4 cells is unaffected by CFIF, being quite high under the culture conditions used here. Experiments, using actinomycin D, daunomycin and cycloheximide showed that the secretion of CFIF from giant cells requires synthesis of RNA and protein. Possibly, cell fusion triggers production of CFIF, which is rapidly released into the external medium.

Biological Products↗
PubMed1991

Possible existence of a light-inducible protein that inhibits sexual cell fusion in Dictyostelium discoideum.

Sexual cell fusion is an initial step of macrocyst formation in Dictyostelium discoideum and requires environmental conditions such as darkness, plenty of water and the presence of calcium ions. We have been analyzing the mechanism of sexual cell fusion between HM1 and NC4, heterothallic strains in D. discoideum. Cells of these strains have been shown to be fusion competent when cultured in a liquid medium in darkness, but not so when cultured on agar plates or in a liquid medium in the light. Two cell-surface proteins, gp70 and gp138, have been identified as target molecules for fusion-blocking antibodies and therefore as relevant to sexual cell fusion. In the present study, gp70 was shown to be present in HM1 cells cultured in the light, and fusion incompetent. Intact HM1 cells cultured in the light were unable to absorb the fusion-blocking activity of antibodies against membrane components of fusion-competent HM1 cells, whose activity had been shown to be absorbed by gp70, but they did so after separation of proteins in the SDS-PAGE. In addition, fusion-competent HM1 cells were found to lose their fusion competence by subsequent cultivation in the light. This loss of competence was cycloheximide sensitive, indicating that de novo synthesis of proteins was necessary for this inhibition. From these results, we presume that light induces a protein that hinders the interaction of gp70 in HM1 cells with its receptor on the NC4 cell surface and thereby inhibits the sexual process between these strains.

Animals↗
PubMed1992

Glycoprotein gI of pseudorabies virus promotes cell fusion and virus spread via direct cell-to-cell transmission.

Mutants of pseudorabies virus defective in either glycoprotein gI or gIII are only slightly less virulent for mice and chickens than is wild-type virus, while mutants defective in both gI and gIII are avirulent. To clarify the reason for the lack of virulence of the gI- gIII- mutants, we have analyzed in some detail the interactions of these mutants with their hosts. The results obtained showed that the gI glycoprotein is an accessory protein that promotes cell fusion. This conclusion is based on the findings that in some cell types, syncytium formation is significantly reduced in mutants deficient in gI. Furthermore, despite efficient replication, gI- mutants form significantly smaller plaques on some cell types. Finally, while wild-type and gI- virus are neutralized similarly by antisera, the size of the plaques formed by gI- mutants, but not by wild-type virus, is reduced by the presence of neutralizing antibodies in the overlay. Passive immunization of mice with neutralizing antipseudorabies virus sera is also considerably more effective in protecting them against challenge with gI- mutants than in protecting them against challenge with wild-type virus. These results show that gI- mutants are deficient in their ability to form syncytia and to spread directly by cell-to-cell transmission and that these mutants spread mainly by adsorption of released virus to uninfected cells. Wild-type virus and gIII- mutants, however, spread mainly via direct cell-to-cell transmission both in vivo and in vitro. We postulate that the lack of virulence of the gIII- gI- virus is attributable to its inability to spread by either mode, the defect in gIII affecting virus spread by adsorption of released virus and the defect in gI affecting cell-to-cell spread. Although a gI- gIII- mutant replicates as well as a gIII- mutant, it will be amplified much less well. Our results with in vitro systems show that this is indeed the case.

Animals↗
PubMed1998

A semiautomated fluorescence-based cell-to-cell fusion assay for gp120-gp41 and CD4 expressing cells.

A novel fluorescence-based method was developed to measure HIV envelope glycoprotein (env)-CD4-mediated cell fusion. This method measures the spread of a fluorescent dye as the cytosolic compartments of adjacent cells become contiguous upon cell-to-cell fusion. Calcein-labeled CD4+ Sup-T1 cells were seeded onto a monolayer of unlabeled TF228.1.16 cells, which stably express env, the gp120-gp41 complex. Changes in the following parameters were measured using a stage-scanning laser microscope: total fluorescent area, average fluorescent area, and average shape factor. Anti-CD4 monoclonal antibodies, anti-Leu3a, and OKT4E were shown to block fusion in a dose-dependent manner, while OKT4 had no effect. Aurin tricarboxylic acid, a compound that interferes with the binding of anti-Leu3a mAb and gp120 to CD4+ human peripheral blood lymphocytes, T20, a peptide that interferes with gp41, and cytochalasin D, a microfilament disrupter, all blocked fusion in a dose-dependent manner. This semiautomated assay can be used to quickly assess the effectiveness of compounds acting at different sites to block CD4 and env initiated cell-to-cell fusion.

Antibodies, Monoclonal↗
PubMed1993

Herpes simplex virus (HSV) glycoproteins B and K inhibit cell fusion induced by HSV syncytial mutants.

Herpes simplex virus type 1 (HSV-1) glycoproteins K and B (gK and gB) are intimately involved in virus-induced fusion of cells. Certain mutations in the UL27 (gB) and UL53 (gK) genes confer a syncytial (syn) phenotype characterized by extensive fusion of infected cells and giving rise to multinucleated cells. We have used HSV-1 syn mutants in conjunction with transfected cells or adenovirus vectors to overexpress wild-type gK or gB, in order to study the role of these proteins in virus-induced membrane fusion. Transient expression of wild-type gK inhibited fusion induced by HSV-1 encoding a mutant form of gK (syn gK) but not by viruses encoding a mutant form of gB (syn gB). Stably transformed cells expressing relatively high levels of gK suppressed cell fusion induced by HSV-1 mutants with lesions in the gK gene but not an HSV-1 with a syn mutation in the gB gene. In addition, there were marked reductions in the plaquing efficiencies and yields of HSV-1 on these cell lines. Cell fusion caused by HSV-1 syn20, a mutant encoding syn gK, was suppressed when cells were coinfected with an Ad vector, AdgK, which expresses wild-type gK. AdgK did not suppress fusion induced by HSV-1 KTTS.1, which expresses syn gB. Conversely, cells coinfected with AdgB, an Ad vector expressing a wild-type form of gB and HSV-1 KTTS.1 (syn gB) were not fused, whereas cells coinfected with AdgB and HSV-1 syn20 (syn gK) were fused. Expression of a number of other HSV-1 glycoproteins using Ad vectors did not reduce membrane fusion induced by syn gK or syn gB. Together, these results support models in which gK and gB participate directly in the fusion of HSV-infected cells. Mutant forms of gB and gK apparently disregulate the fusion process, whereas wild-type forms of gB and gK can act to suppress membrane fusion induced by their mutant counterparts.

Adenoviridae↗
PubMed2006

Study on biological characters of SGC7901 gastric cancer cell-dendritic cell fusion vaccines.

AIM: To detect the biological characters of the SGC7901 gastric cancer cell-dendritic cell fusion vaccines. METHODS: The suspending living SGC7901 gastric cancer cells and dendritic cells were induced to be fusioned by polyethylene glycol. Pure fusion cells were obtained by selective culture with the HAT/HT culture systems. The fusion cells were counted at different time points of culture and their growth curves were drawn to reflect their proliferative activities. The fusion cells were also cultured in culture medium to investigate whether they could grow into cell clones. MTT method was used to test the stimulating abilities of the fusion cells on T lymphocytes' proliferations. Moreover, the fusion cells were planted into nude mice to observe whether they could grow into new planted tumors in this kind of immunodeficiency animals. RESULTS: The fusion cells had weaker proliferative activity and clone abilities than their parental cells. When they were cultured, the counts of cells did not increase remarkably, nor could they grow into cell clones in culture medium. The fusion cells could not grow into new planted tumors after planted into nude mice. The stimulating abilities of the fusion cells on T lymphocytes' proliferations were remarkably increased than their parental dendritic cells. CONCLUSION: The SGC7901 gastric cancer cell-dendritic cell fusion vaccines have much weaker proliferative abilities than their parental cells, but they keep strong abilities to irritate the T lymphocytes and have no abilities to grow into new planted tumors in immunodeficiency animals. These are the biological basis for their anti-tumor biotherapies.

Animals↗
PubMed2004

Detection of osteoclastic cell-cell fusion through retroviral vector packaging.

Cell-cell fusion generates multinucleated cells such as osteoclasts in bone, myotubes in muscle, and trophoblasts in placenta. Molecular details governing these fusion processes are still largely unknown. As a step toward identification of fusogenic genes, we tested the concept that retroviral vectors can be packaged as a result of cell-cell fusion. First, we introduced replication-deficient retroviral vectors expressing mCAT-1, which mediates fusogenic interaction with the retroviral envelope protein Env, into Chinese hamster ovary (CHO) cells to generate vector cells. Plasmids expressing virion proteins Gag, Pol, and Env were introduced into a separate culture of CHO cells to generate packaging cells. Co-culturing vector and packaging cells resulted in production of infectious retroviruses carrying the mCAT-1 gene as a consequence of cell-cell fusion. Second, we introduced a retroviral vector into primary osteoclast precursors and co-cultured them with established osteoclast precursor RAW264.7 cells, which turned out to harbor packaging activity. Packaged retroviral vector was detected in culture supernatants only where the osteoclast differentiation factor receptor activator for NF-kappaB ligand (RANKL) induced fusion between these two cell types. These data suggest that retrovirus production can occur as a result of cell-cell fusion. This provides a novel approach for isolating and characterizing fusogenic genes using retroviral expression vectors.

Animals↗
PubMed1984

Ultrastructure of the fusion cell in Faucheocolax attenuata Setch. (Rhodophyta, Rhodymeniales).

The fusion cell in Faucheocolax attenuata Setch. is a highly lobed, thick-walled, multinucleate and irregularly shaped cell originating from the basal cell of the auxiliary cell branch. The formation of the fusion cell occurs by an incorporation of vegetative cells into the basal cell, after dissolution of septal plugs between these cell types. Thus the fusion cell is a syncytium containing only haploid nuclei, as well as unusual mitochondria and plastids. Mitochondria lack cristae and instead contain a tubular helical structure. Plastids are atypical with regard to thylakoid organization in red algae, because they lack the peripheral thylakoid and their photosynthetic thylakoids are aggregated to one side. In addition, they contain large osmiophilic bodies. Nuclear envelopes appear to produce large quantities of membrane cisternae. Floridean starch is absent and the cytoplasm contains few ribosomes. The plasma membrane is irregular and endoplasmic reticulum cisternae are situated parallel to it. Bundles of putative microfilaments were commonly found in nuclei and the cytoplasm. Structural evidence does not support any meristematic, nutritive or secretory functions previously ascribed to fusion cells in other genera.

Cell Fusion↗
PubMed1999

Dpp and Notch specify the fusion cell fate in the dorsal branches of the Drosophila trachea.

Decapentaplegic (Dpp) signaling determines the number of cells that migrate dorsally to form the dorsal primary branch during tracheal development. We report that Dpp signaling is also required for the differentiation of one of three different cell types in the dorsal branches, the fusion cell. In Mad mutant embryos or in embryos expressing dominant negative constructs of the two type I Dpp receptors in the trachea the number of cells expressing fusion cell-specific marker genes is reduced and fusion of the dorsal branches is defective. Ectopic expression of Dpp or the activated form of the Dpp receptor Tkv in all tracheal cells induces ectopic fusions of the tracheal lumen and ectopic expression of fusion gene markers in all tracheal branches. Among the fusion marker genes that are activated in the trachea in response to ectopic Dpp signaling is Delta. In conditional Notch loss of function mutants additional tracheal cells adopt the fusion cell fate and ectopic expression of an activated form of the Notch receptor in fusion cells results in suppression of fusion cell markers and disruption of the branch fusion. The number of cells that express the fusion cell markers in response to ectopic Dpp signaling is increased in Notch(ts1) mutants, suggesting that the two signaling pathways have opposing effects in the selection of the fusion cells in the dorsal branches.

Animals↗
PubMedDate not supplied

[Can postradiation cell fusion be a factor in the protection of a cell population?].

From the analysis of the literature it is inferred that there is one more type of nonspecific protection which is based on the polyploidy process and functions at the cell population and tissue levels. With high radiation loads, this process maintains the functioning rate of the given tissue and the survival rate of the given cell type. A hypothesis is proposed that cell fusion and formation of somatic hybrids, that provide clone survival, are particularly effective in tumor tissues. This mechanism is activated at high radiation doses: fusion of injured cells and formation of polykaryons and then hybrids can give rise to cells capable of reproduction. The cellularity is restored.

Animals↗