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At least 91 records · Page 5Linked to original sources
PubMed1981

Monoclonal antibodies to carcinoembryonic antigen produced by somatic cell fusion.

Hybridoma cell lines secreting monoclonal antibodies to carcinoembryonic antigen (CEA) were generated by fusing mouse immune lymphocytes with the mouse myeloma variant cell line, NS-1. Antibody secreted by one cloned hybrid cell line could bind only a select portion of the CEA bound by the commercially available goat anti-CEA antiserum used in clinical assays. Radiolabeled CEA could be purified on a monoclonal antibody affinity column. Incorporation of this purified radiolabeled CEA in a double-antibody solid-phase assay with goat anti-CEA antiserum led to an approximately 2.5-fold increase in sensitivity of the assay. Genetically stable hybrid clones may be sources of virtually unlimited quantities of such antibodies which may have potential utility in improving the cancer specificity of clinical assays.

Animals↗
PubMed1997

Promonocytic U937 subclones expressing CD4 and CXCR4 are resistant to infection with and cell-to-cell fusion by T-cell-tropic human immunodeficiency virus type 1.

Different strains of human immunodeficiency virus type 1 (HIV-1) vary markedly in the ability to infect cells of the monocyte/macrophage (M/M) lineage. M/M are generally resistant to infection with T-cell-tropic (T-tropic) strains of HIV-1. Recently, the chemokine receptors CCR5 and CXCR4 were identified as cofactors for fusion/entry of macrophage- and T-tropic strains of HIV-1, respectively. To investigate the mechanisms of resistance of M/M to T-tropic HIV-1 infection, we examined a number of subclones of the U937 promonocytic cell line. We found that certain subclones of U937 (plus clones) could, while others (minus clones) could not, support replication of T-tropic strains of HIV-1. We demonstrate that (i) both minus and plus clones support HIV-1 replication when transfected with an infectious molecular cDNA clone of a T-tropic HIV-1; (ii) minus clones do not, but plus clones do, efficiently support fusion with cells expressing HIV-1 IIIB Env; (iii) both plus and minus clones (with the exception of one clone) express physiologically functional CXCR4 protein as well as CD4 on the cell surface; (iv) introduction of CXCR4 into the CXCR4-negative clone does not restore fusogenicity with or susceptibility to T-tropic HIV-1; and (v) a ligand (stromal cell-derived factor 1) for or a monoclonal antibody (12G5) to CXCR4 does not effectively inhibit HIV-mediated cell-to-cell fusion of U937 cells. These data indicate that resistance to T-tropic HIV-1 infection of U937 minus clones occurs at fusion/ entry events and that expression of functional CXCR4 and CD4 is not a sole determinant for susceptibility to T-tropic HIV-1 infection; furthermore, they suggest that other factors are positively or negatively involved in HIV-mediated cell-to-cell fusion in U937 promonocytic cells.

Antibodies↗
PubMed1982

The isolation and characterization of mutants of herpes simplex virus type 1 that induce cell fusion.

Six cell fusion-causing syn mutants were isolated from the KOS (syn-101 to syn-106) and three from the HFEM (syn-109) strains of herpes simplex virus type 1 (HSV-1). The mutants were studied by complementation and recombination with syn-20 (a syncytial mutant of KOS) and ts-B5 (a syncytial mutant of HFEM). Some studies also employed MP, a syncytium-inducing strain isolated from the non-syncytial parent, mP. Complementation and recombination of syn-20 and ts-B5 indicated that these two mutants were altered in two different virus genes. The recombination frequency between syn-20 and ts-B5 was very similar to that observed between MP and ts-B5, indicating the syn-20 and MP may represent alterations in the same virus gene. syn-101, syn-103, syn-104 and syn-105 were tentatively assigned to the syn-20 complementation group, while syn-107 and syn-109 were tentatively assigned to the ts-B5 complementation group, syn-106 and syn-108 were excluded from the ts-B5 group. syn-102 could not be excluded from either complementation group. syn-101 induced markedly less fusion at 38 degrees C relative to 34 degrees C. At 34 degrees C the patterns of syn-101-infected cell peptides and glycopeptides, examined by SDS-gel electrophoresis, were normal, but at 38 degrees C the amount of glycopeptide gC was particularly reduced. syn-102 produced decreased amounts of glycoproteins, and a non-glycosylated peptide, probably ICP6, was absent from extracts infected with syn-106.

Cell Fusion↗
PubMed2004

Membrane potential and endocytic activity control disintegration of cell-cell adhesion and cell fusion in vinculin-injected MDBK cells.

Cell fusion occurs during fertilization and in the formation of organs such as muscles, placenta, and bones. We have developed an experimental model for epithelial cell fusion which permits analysis of the processes during junction disintegration and formation of polykaryons (Palovuori and Eskelinen [2000] Eur. J. Cell. Biol. 79: 961-974). In the present work, we analyzed the process in detail. Cell fusion was achieved by microinjecting into the cytoplasm of kidney epithelial Madin-Darby bovine kidney (MDBK) cells TAMRA-tagged vinculin, which incorporated into lateral membranes, focal adhesions and nucleus, and, prior fusion, induced internalization of actin, cadherin and plakoglobin to small clusters in cytoplasm. Injected vinculin was still visible at lateral membranes after removal of junctional proteins indicating that it was tightly associated and perturbed the cell-cell contact sites resulting in membrane fragmentation. Injection of active Rac together with vinculin induced accumulation of cadherin to the membranes, but did not affect vinculin-membrane association. However, it hampered cell fusion probably by supporting adherens junctions. In order to stop endocytosis, we lowered intracellular pH of vinculin-injected cells to 5.5 with the aid of nigericin in KCl buffer. In acidified cells, injected vinculin delineated lateral membranes as thick layers, cadherin remained in situ, and cell fusion was completely inhibited. Since this treatment also leads to cell depolarization, we checked the vinculin incorporation in a KCl solution containing nigericin at neutral pH. In these circumstances, both endogenous and injected vinculin delineated lateral membranes as very thin discontinuous layers, but still fusion was hampered most likely due to perturbation in the initial vinculin-membrane association. We suggest that vinculin might function as a sensor of the environment triggering cell fusion during development in circumstances where membrane potential and local and transient pH gradients play a role.

Adherens Junctions↗
PubMed1987

Induction of cell fusion in Newcastle disease virus-infected L929 cells by anti-L929 cell antisera.

Infection of L929 cells by Newcastle disease virus (NDV) did not induce cell fusion, whereas addition of anti-L929 cell antiserum to the culture medium did result in cell fusion. When the antiserum was added to the culture medium of NDV-infected cells at the start of incubation, polykaryocytes appeared after 18 h post-infection (p.i.). On the other hand, when the antiserum was added to the culture medium at 18 h p.i., no polykaryocytes appeared, suggesting that the presence of the antiserum at the stage of NDV replication was necessary for the antiserum-induced cell fusion. Since anti-F polypeptide antiserum inhibited the cell fusion, functional F protein was essential for the antiserum-induced cell fusion. All the anti-L929 cell xenogenic sera tested were able to induce the cell fusion, whereas anti-L929 cell allogenic sera did not induce cell fusion. Anti-MCA cell serum also induced the cell fusion. Little replication of NDV was observed in the presence of anti-L929 cell serum and synthesis of virus-specific polypeptides, especially of M protein, was suppressed. However, there was no difference in expression of virus-specific glycoproteins on the surface membranes between cells treated with normal rabbit serum and those treated with anti-L929 cell serum. On the basis of the above results, the mechanism of induction of cell fusion by anti-host cell serum is discussed.

Animals↗
PubMed1987

A novel method for the detection of early events in cell-cell fusion of Semliki Forest virus infected cells growing in monolayer cultures.

Semliki Forest virus infected Aedes albopictus cells were used to investigate virus induced cell-cell fusion. It was shown by a novel method that cell-cell fusion was completed within approximately 5 minutes after triggering the fusion event by low pH. This method consists of fixing fusing cells with glutaraldehyde and microinjecting the highly fluorescent and rapidly diffusing dye Lucifer yellow. In contrast, polykaryon formation, the usually used criterion to measure cell-cell fusion occurred only within 30 minutes. Furthermore, it was shown that potassium cyanide, a potent inhibitor of polykaryon formation in the described system, inhibits an early step of membrane-membrane fusion of neighbouring cells.

Aedes↗
PubMed1994

Herpesvirus-induced cell fusion that is dependent on cell surface heparan sulfate or soluble heparin.

The entry of enveloped viruses into animal cells and the cell-to-cell spread of infection via cell fusion require the membrane-fusing activity of viral glycoproteins. This activity can be dependent on variable cell factors or triggered by environmental factors. Here we show that cell fusion induced by herpes simplex virus glycoproteins is dependent on the presence of cell surface glycosaminoglycans, principally heparan sulfate, or on the addition of heparin to the medium. The role of the glycosaminoglycan is probably to alter the conformation of a viral heparin-binding glycoprotein required for the fusion.

Animals↗
PubMed2026

Live dynamics of induced cell-cell fusion between mitotic and interphasic cells.

The cell cycle is tightly regulated by checkpoint mechanisms that ensure faithful duplication and segregation of the genome. Here, we induced cell-cell fusion between mitotic and interphase cells to study how nuclei from different cell cycle stages behave in a shared cytoplasm. We found that mitosis is a dominant cell cycle state: the mitotic cytoplasm can drive interphase nuclei into mitosis, whereas, in high ratios of interphase versus mitotic nuclei, fusion forced mitotic nuclei to exit mitosis. Both outcomes represent checkpoint override events with impactful consequences. Interphase nuclei forced into mitosis form aberrant mitotic spindles, show partially condensed DNA and ultimately undergo mitotic catastrophe. Conversely, forced mitotic exit resulted in reformation of nuclear envelope membranes around condensed chromosomes, forming nuclei with a defective nuclear import machinery. Altogether, cell-cell fusion revealed the consequences of checkpoint override, forcing nuclei through untimely cell cycle transitions, and highlight how cell-cell fusion experiments can be a powerful system to study how competing cytoplasmic states are integrated in a shared cytoplasm, such as in muscle, placenta formation and in cancer.

Cell cycle↗
PubMed2006

Paramyxovirus fusion: real-time measurement of parainfluenza virus 5 virus-cell fusion.

Although cell-cell fusion assays are useful surrogate methods for studying virus fusion, differences between cell-cell and virus-cell fusion exist. To examine paramyxovirus fusion in real time, we labeled viruses with fluorescent lipid probes and monitored virus-cell fusion by fluorimetry. Two parainfluenza virus 5 (PIV5) isolates (W3A and SER) and PIV5 containing mutations within the fusion protein (F) were studied. Fusion was specific and temperature-dependent. Compared to many low pH-dependent viruses, the kinetics of PIV5 fusion was slow, approaching completion within several minutes. As predicted from cell-cell fusion assays, virus containing an F protein with an extended cytoplasmic tail (rSV5 F551) had reduced fusion compared to wild-type virus (W3A). In contrast, virus-cell fusion for SER occurred at near wild-type levels, despite the fact that this isolate exhibits a severely reduced cell-cell fusion phenotype. These results support the notion that virus-cell and cell-cell fusion have significant differences.

Animals↗
PubMed2006

Syncytin is involved in breast cancer-endothelial cell fusions.

Cancer cells can fuse spontaneously with normal host cells, including endothelial cells, and such fusions may strongly modulate the biological behaviour of tumors. However, the underlying mechanisms are unknown. We now show that human breast cancer cell lines and 63 out of 165 (38%) breast cancer specimens express syncytin, an endogenous retroviral envelope protein, previously implicated in fusions between placental trophoblast cells. Additionally, endothelial and cancer cells are shown to express ASCT-2, a receptor for syncytin. Syncytin antisense treatment decreases syncytin expression and inhibits fusions between breast cancer cells and endothelial cells. Moreover, a syncytin inhibitory peptide also inhibits fusions between cancer and endothelial cells. These results are the first to show that syncytin is expressed by human cancer cells and is involved in cancer-endothelial cell fusions.

Amino Acid Transport System ASC↗
PubMed1990

Expression of bovine herpesvirus type 1 glycoprotein gI in transfected bovine cells induces spontaneous cell fusion.

Bovine MDBK cells were transfected with Rous sarcoma virus-based vectors for constitutive expression of the bovine herpesvirus type 1 (BHV-1) glycoprotein, gI. Cell lines stably expressing recombinant gI were cloned and characterized. Recombinant gI was localized intracellularly, predominantly in a perinuclear region, and on the cell surface. Cells expressing gI exhibited spontaneous polykaryon formation, thus confirming the fusogenic activity described previously in gI-expressing transfected murine LMTK- cells. The recombinant form of gI synthesized in transfected MDBK cells was similar in Mr to the form expressed in BHV-1-infected MDBK cells, unlike the recombinant form of gI expressed by LMTK- cells which is deficient in N-linked glycosylation. It was concluded that cell fusion associated with the expression of BHV-1 gI in transfected mammalian cells is a reproducible phenomenon in a number of cell types and is not due to species-specific factors or expression of abnormally glycosylated gI. Cell fusion is a useful in vitro marker for gI function and may contribute to the spread of BHV-1 infections in vivo.

Animals↗
PubMed1999

Amino acid substitutions at position 481 differently affect the ability of the measles virus hemagglutinin to induce cell fusion in monkey and marmoset cells co-expressing the fusion protein.

The hemagglutinin (H) protein of the measles virus (MV) Edmonston strain induced cell fusion in Cos (monkey) and B95a (marmoset) cells, when co-expressed with the fusion (F) protein, whereas the H protein of the wild-type KA strain induced fusion in B95a cells, but not in Cos cells. Asparagine residue at position 481 of the KA H protein was replaced by various amino acids through site-directed mutagenesis. Substitution with tyrosine, which was found at position 481 of the Edmonston H protein, enabled the mutant KA H protein (N481Y) to induce cell fusion in Cos cells co-expressing the F protein, which could be completely blocked by anti-CD46 antibody. This mutant, however, did not cause CD46 downregulation, unlike the Edmonston H protein. The other H protein mutants (N481S, N481T, N481D, N481H, N481F) did not produce syncytia in Cos cells. On the other hand, all of the mutants retained the ability to induce cell fusion in B95a cells. Thus, while tyrosine at position 481 was indispensable for the MV H protein's interaction with CD46, the residue at this position does not appear to be critically involved in the interaction with the receptor for wild-type strains present on B95a cells.

Amino Acid Substitution↗
PubMed1977

Studies of membrane fusion. I. Paramyxovirus-induced cell fusion, a scanning electron-microscope study.

Fusion of erythrocytes and HeLa cells with Sendai and Newcastle disease viruses has been studied by scanning electron microscopy. Most virus particles are spherical but vary in diameter from approximately 200 to approximately 600 nm. At 4 degrees C virus particles bind randomly to the cell surface and at high cell densities cross-linking of adjacent cells by virus particles results in cell agglutination. Cell-cell fusion takes place when the agglutinated cell suspension is warmed to 37 degrees C. Fusion is initiated at sites of cell-cell contact and is accompanied in all cases by cell swelling. In the case of suspension HeLa cells, virally mediated cell swelling involves an 'unfolding' of cell surface microvilli and results in the formation of smooth-surfaced single or fused cells. With erythrocytes, swelling results in haemolysis. There is a dramatic reduction in the numbers of virus particles bound to cells following fusion.

Cell Aggregation↗
PubMed2000

Fusomorphogenesis: cell fusion in organ formation.

Cell fusion is a universal process that occurs during fertilization and in the formation of organs such as muscles, placenta, and bones. Very little is known about the molecular and cellular mechanisms of cell fusion during pattern formation. Here we review the dynamic anatomy of all cell fusions during embryonic and postembryonic development in an organism. Nearly all the cell fates and cell lineages are invariant in the nematode C. elegans and one third of the cells that are born fuse to form 44 syncytia in a reproducible and stereotyped way. To explain the function of cell fusion in organ formation we propose the fusomorphogenetic model as a simple cellular mechanism to efficiently redistribute membranes using a combination of cell fusion and polarized membrane recycling during morphogenesis. Thus, regulated intercellular and intracellular membrane fusion processes may drive elongation of the embryo as well as postembryonic organ formation in C. elegans. Finally, we use the fusomorphogenetic hypothesis to explain the role of cell fusion in the formation of organs like muscles, bones, and placenta in mammals and other species and to speculate on how the intracellular machinery that drive fusomorphogenesis may have evolved.

Animals↗
PubMed2001

Effects of cyclosporin A on cell fusion in a monkey kidney cell line persistently infected with measles virus.

The authors studied the effects of immunosuppressive peptide cyclosporin A (CsA) on cell fusion efficiency in cells persistently infected with measles virus (448-PI-Vero cells). Treatment of 448-PI-Vero cells with 5 microM CsA enhanced the infusion. In addition, the expression of measles virus antigen on cell surface was increased by treatment with CsA. The addition of phenothiazine, an anti-calmodulin drug, enhanced the fusion of 448-PI-Vero cells in the presence of CsA, although treatment with phenothiazine alone did not affect polykaryocyte formation. The enhancement of fusion efficiency in 448-PI-Vero cells by CsA was suppressed by oligopeptide Z-D-Phe-Phe-Gly, a synthetic oligopeptide that inhibits fusion induced by measles virus. Since the cell content of major virus-specific polypeptides, such as hemagglutinin, nucleoprotein or matrix protein is the same as in untreated controls, this fusion enhancement may be related to transport and accumulation of measles virus glycoproteins.

Animals↗