Respiratory syncytial virus (RSV) induces the production of a number of cytokines and chemokines by activation of nuclear factor kappa B (NF-kappaB). The activation of NF-kappaB has been shown to depend on viral replication in the infected cells. In this study, we demonstrate that expression of RSV M2-1 protein, a transcriptional processivity and anti-termination factor, is sufficient to activate NF-kappaB in A549 cells. Electromobility shift assays show increased NF-kappaB complexes in the nuclei of M2-1-expressing cells. M2-1 protein is found in nuclei of M2-1-expressing cells and in RSV-infected cells. Co-immunoprecipitations of nuclear extracts of M2-1-expressing cells and of RSV-infected cells revealed an association of M2-1 with Rel A protein. Furthermore, the activation of NF-kappaB depends on the C-terminus of the RSV M2-1 protein, as shown by NF-kappaB-induced gene expression of a reporter gene construct.
The fiber cells of the middle layer of Trichoplax adhaerens are interconnected by slender extensions. Newly formed connections after mechanical disruption of the tissue studied in ultrathin sections revealed cytoplasmic continuity between the cell bodies, suggesting a syncytial organisation of the fiber cell layer. The slender extensions connecting the cell bodies are traversed by microtubules and microfilaments. The structure of rare osmiophilic cell contacts suggests a stage in the fusion of adjacent cell membranes.
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