Analysis of uridine incorporation in chicken embryo cells infected by vesicular stomatitis virus and its temperature-sensitive mutants: uridine transport.
The shut-off of RNA synthesis in chicken embryo cells, after infection with vesicular stomatitis virus, is partially due to a reduced capacity of the infected cells to transport uridine. Permeability to uridine decreases exponentially after infection. This loss of ability to transport uridine may be caused either by structural components of the input virions or may result from the expression of the viral gene products. In the latter case, only minor levels of viral transcription is sufficient to modify cellular permeability, since, even at low multiplicities, RNA minus temperature-sensitive (ts) mutants of vesicular stomatitis virus bring about a significant diminution of uridine incorporation in cells infected under nonpermissive conditions. Experiments with mutants of group III suggest that the M protein of the viral envelope may play a role in the sequence of events that modifies uridine transport. In addition to this cause of the diminution of incorporation of uridine by infected cells, another mechanism is noted which requires protein synthesis.
D000818:Animals; D001693:Biological Transport, Active; D002463:Cell Membrane Permeability; D002478:Cells, Cultured; D002642:Chick Embryo; D003513:Cycloheximide / Q000494:pharmacology; D006207:Half-Life; D009154:Mutation; D012313:RNA / Q000096:biosynthesis; D011830:Radiation Effects; D013696:Temperature; D014316:Tritium; D014466:Ultraviolet Rays; D014529:Uridine / Q000378:metabolism*; D014721:Vesicular stomatitis Indiana virus / Q000254:growth & development* / Q000528:radiation effects
D014316:Tritium; D012313:RNA; D003513:Cycloheximide; D014529:Uridine