title: Vesicular stomatitis virus P function depends on cellular growth cycle.
abstract: The P function of vesicular stomatitis virus (VSV) is defined as the viral function which results in a reduced rate of total protein synthesis (viral plus cellular) arising from a nonspecific reduction in the efficiency of the translational machinery in infected cells. The existence of P function has been challenged by Lodish and Porter who were unable to detect it in L-strain mouse cells infected with wild-type VSV (HR) or, as expected, with the P- mutant, T1026-R1. Although other groups have subsequently confirmed the existence of P function and the difference between HR and T1026-R1, we have sought an explanation for the difference between Lodish and Porter's results and those of other laboratories. We show that the VSV P function depends on the phase of the growth cycle of infected L-cell cultures. In very early exponential phase, as used by Lodish and Porter, HR has very little demonstrable P function; as the growth cycle proceeds toward stationary phase, P function becomes more and more manifest. Under the same conditions, T1026-R1 shows no P function throughout the growth cycle. Furthermore we show that the VSV M protein mutant tsG31 has a P++ phenotype reducing total protein synthesis below that seen with wild-type HR. P function can be observed in cells infected with tsG31, even early in the exponential phase of the cellular growth cycle.
authors.forename: C P
authors.initials: CP
authors.lastname: Stanners
authors.forename: S
authors.initials: S
authors.lastname: Kennedy
authors.forename: L
authors.initials: L
authors.lastname: Poliquin
mesh_terms: D000818:Animals; D002453:Cell Cycle; D005786:Gene Expression Regulation; D007739:L Cells / Q000382:microbiology / Q000502:physiology*; D051379:Mice; D014176:Protein Biosynthesis; D014721:Vesicular stomatitis Indiana virus / Q000235:genetics / Q000502:physiology*