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A polyoma mutant that encodes small T antigen but not middle T antigen demonstrates uncoupling of cell surface and

T J Liang, G G Carmichael, T L Benjamin

    Molecular and Cellular Biology
    |December 1, 1984
    PubMed

    Insights

    Polyoma virus middle T antigen is not required for all cellular changes associated with oncogenesis. A mutant virus, Py808A, shows that middle T antigen is separable from cell surface agglutination and cytoskeletal changes.

    Area of Science:

    • Virology
    • Molecular Biology
    • Cell Biology

    Background:

    • The hr-t gene in polyoma virus is crucial for encoding small and middle T antigens, which have diverse cellular effects.
    • Middle T antigen is implicated in cellular transformation and alterations in cell structure.

    Purpose of the Study:

    • To investigate the specific roles of middle T antigen in polyoma virus-induced cellular changes.
    • To determine if structural changes at the cell surface are linked to cytoskeletal and extracellular matrix alterations.

    Main Methods:

    • Construction of a polyoma virus mutant (Py808A) by mutating the 3' splice site for middle T mRNA.
    • Analysis of Py808A's ability to induce morphological transformation, anchorage-independent growth, and postconfluent growth.
    • Assessment of cell agglutinability by lectins, actin cable architecture, and extracellular fibronectin levels in infected cells.

    Main Results:

    • Py808A mutant expressed normal small and large T proteins but lacked middle T protein.
    • The mutant failed to induce morphological transformation or soft agar growth but stimulated postconfluent growth.
    • Cells infected with Py808A showed increased lectin agglutinability while maintaining normal actin cables and fibronectin levels.

    Conclusions:

    • Middle T antigen is not essential for all oncogenic effects of polyoma virus.
    • Py808A demonstrates that cell surface structural changes (agglutination) can be separated from cytoskeletal and extracellular matrix alterations.
    • This finding decouples previously linked parameters in viral oncogenesis.

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