Changing Epstein-Barr viral ZEBRA protein into a more powerful activator enhances its capacity to disrupt latency.
The Epstein-Barr viral transcriptional activator ZEBRA induces expression of viral early lytic genes when introduced into cells bearing latent Epstein-Barr virus. We show here that a ZEBRA-herpes simplex viral protein 16 (VP16) fusion protein induces early viral lytic gene expression in Epstein-Barr virus-containing cells more efficiently than does wild-type ZEBRA. The fusion protein is also a more powerful transcriptional activator in these cells, as assayed with reporter constructs. Our experiments also suggest that ZEBRA manifests a function required for full activity on certain natural promoters but not on promoters bearing oligomerized ZEBRA binding sites; this function cannot be provided by VP16.
Department of Molecular Biophysics and Biochemistry, Yale University, New Haven, CT 06510.
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Baumann
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Grogan
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Ptashne
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Miller
D002478:Cells, Cultured; D004268:DNA-Binding Proteins / Q000378:metabolism / Q000502:physiology*; D015967:Gene Expression Regulation, Viral; D004854:Herpesvirus 4, Human / Q000472:pathogenicity*; D006801:Humans; D066298:In Vitro Techniques; D011485:Protein Binding; D012333:RNA, Messenger / Q000235:genetics; D011993:Recombinant Fusion Proteins / Q000235:genetics; D013329:Structure-Activity Relationship; D015534:Trans-Activators / Q000502:physiology*; D014157:Transcription Factors / Q000235:genetics / Q000378:metabolism; D015533:Transcriptional Activation; D014764:Viral Proteins; D014779:Virus Replication
C063676:BZLF1 protein, Herpesvirus 4, Human; D004268:DNA-Binding Proteins; D012333:RNA, Messenger; D011993:Recombinant Fusion Proteins; D015534:Trans-Activators; D014157:Transcription Factors; D014764:Viral Proteins