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Related Experiment Videos

Vesicular stomatitis virus P function depends on cellular growth cycle.

C P Stanners, S Kennedy, L Poliquin

    Virology
    |September 1, 1987
    PubMed
    Summary
    This summary is machine-generated.

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    Vesicular stomatitis virus (VSV) P function, which reduces protein synthesis, is dependent on the cell

    Area of Science:

    • Virology
    • Molecular Biology
    • Cell Biology

    Background:

    • The P function of vesicular stomatitis virus (VSV) is characterized by reduced total protein synthesis in infected cells due to decreased translational machinery efficiency.
    • The existence and detectability of VSV P function have been debated, with conflicting results between laboratories regarding wild-type VSV (HR) and a P- mutant (T1026-R1).

    Purpose of the Study:

    • To investigate the discrepancy in VSV P function detection between different laboratories.
    • To elucidate the factors influencing the manifestation of VSV P function in infected cells.

    Main Methods:

    • Infection of L-cell cultures with VSV strains (HR, T1026-R1, tsG31) at different growth phases (exponential, stationary).
    • Analysis of total protein synthesis rates in infected cells.

    Related Experiment Videos

  • Characterization of the P function phenotype (P+, P-, P++) based on protein synthesis reduction.
  • Main Results:

    • VSV P function is dependent on the growth phase of infected L-cell cultures; it is less apparent in early exponential phase and more pronounced in stationary phase.
    • The VSV P- mutant T1026-R1 consistently lacks P function across all growth phases.
    • A VSV M protein mutant, tsG31, exhibits a P++ phenotype, causing a greater reduction in protein synthesis than wild-type HR, and displays P function even in early exponential phase cells.

    Conclusions:

    • The detectability of VSV P function is significantly influenced by the cellular growth phase.
    • VSV P function is not universally absent in early exponential phase cells, contrary to previous findings.
    • The M protein plays a role in the P function phenotype, with the tsG31 mutant demonstrating a distinct and potent effect on protein synthesis.