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The major immediate-early (MIE) gene of human cytomegalovirus (HCMV) encodes several MIE proteins (MIEPs) produced as a result of alternative splicing and polyadenylation of the primary transcript. Previously we demonstrated that the HCMV MIEPs expressed from the entire MIE gene could rescue the temperature-sensitive (ts ) transcriptional defect in thets 13 cell line. This defect is caused by ats mutation in TAFII 250, the 250-kDa TATA binding protein-associated factor (TAF). These and other data suggested that the MIEPs perform a TAF-like function in complex with the basal transcription factor TFIID. In addition to the transcriptional defect, thets mutation ints 13 cells results in a defect in cell cycle progression which ultimately leads to apoptosis. Since all of these defects can be rescued by wild-type TAFII 250, we asked whether the MIEPs could rescue the cell cycle defect and/or affect the progression to apoptosis. We have found that the MIEPs, expressed from the entire MIE gene, do not rescue the cell cycle block ints 13 cells grown at the nonpermissive temperature. However, despite the maintenance of the cell cycle block, thets 13 cells which express the MIEPs are resistant to apoptosis. MIEP mutants, which have previously been shown to be defective in rescuing thets transcriptional defect, maintained the ability to inhibit apoptosis. Hence, the MIEP functions which affect transcription appear to be separable from the functions which inhibit apoptosis. We discuss these data in the light of the HCMV life cycle and the possibility that the MIEPs promote cellular transformation by a “hit-and-run” mechanism.

journal of virology

Effects of Human Cytomegalovirus Major Immediate-Early Proteins in Controlling the Cell Cycle and Inhibiting Apoptosis: Studies with <i>ts</i> 13 Cells

Effects of Human Cytomegalovirus Major Immediate-Early Proteins in Controlling the Cell Cycle and Inhibiting Apoptosis: Studies with ts 13 Cells