Multiple EBNA1-binding sites are required to form an EBNA1-dependent enhancer and to activate a minimal replicative origin within oriP of Epstein-Barr virus - PubMed (original) (raw)

Multiple EBNA1-binding sites are required to form an EBNA1-dependent enhancer and to activate a minimal replicative origin within oriP of Epstein-Barr virus

D A Wysokenski et al. J Virol. 1989 Jun.

Abstract

EBNA1 activates the EBV plasmid maintenance sequence oriP by binding to its two essential regions. One region is a family of 30-base-pair (bp) repeats and is activated by EBNA1 to act as a transcriptional enhancer. The other region contains a 65-bp dyad symmetry and lacks enhancer function. To explore the functional differences between the two regions, we determined oriP activities as functions of the number of 30-bp repeats and compared them with activities determined when tandem copies of the dyad symmetry region were used to replace the 30-bp repeats. Three conclusions have been drawn. (i) Activation of the 30-bp repeats by EBNA1 to enhance transcription or to permit plasmid maintenance is a highly cooperative process involving at least six or seven 30-bp repeats for full activity. (ii) Tandem copies of the dyad symmetry region cooperatively enhance transcription but are less effective than 30-bp repeats providing a similar number of EBNA1-binding sites. (iii) Tandem copies of the dyad symmetry region alone cooperatively activate replication, suggesting that the region contains the actual origin of replication. We also report that while rodent-derived cell lines do not support replication of EBV-derived plasmids they do permit EBNA1-dependent enhancer activity. EBV plasmid replication thus requires the interaction of EBNA1 or oriP with a host factor that is not required for enhancement of transcription.

PubMed Disclaimer

Cited by

The minimal replicator element of the Kaposi's sarcoma-associated herpesvirus terminal repeat supports replication in a semiconservative and cell-cycle-dependent manner.
Verma SC, Choudhuri T, Robertson ES. Verma SC, et al. J Virol. 2007 Apr;81(7):3402-13. doi: 10.1128/JVI.01607-06. Epub 2006 Dec 6. J Virol. 2007. PMID: 17151118 Free PMC article.
Phosphoacceptor site S173 in the regulatory domain of Epstein-Barr Virus ZEBRA protein is required for lytic DNA replication but not for activation of viral early genes.
El-Guindy A, Heston L, Delecluse HJ, Miller G. El-Guindy A, et al. J Virol. 2007 Apr;81(7):3303-16. doi: 10.1128/JVI.02445-06. Epub 2007 Jan 10. J Virol. 2007. PMID: 17215287 Free PMC article.
Epstein-Barr virus nuclear antigen 1 does not induce lymphoma in transgenic FVB mice.
Kang MS, Lu H, Yasui T, Sharpe A, Warren H, Cahir-McFarland E, Bronson R, Hung SC, Kieff E. Kang MS, et al. Proc Natl Acad Sci U S A. 2005 Jan 18;102(3):820-5. doi: 10.1073/pnas.0408774102. Epub 2005 Jan 7. Proc Natl Acad Sci U S A. 2005. PMID: 15640350 Free PMC article.
The Critical Role of Genome Maintenance Proteins in Immune Evasion During Gammaherpesvirus Latency.
Sorel O, Dewals BG. Sorel O, et al. Front Microbiol. 2019 Jan 9;9:3315. doi: 10.3389/fmicb.2018.03315. eCollection 2018. Front Microbiol. 2019. PMID: 30687291 Free PMC article. Review.
Epstein-Barr virus-derived vector suitable for long-term expression in neurons.
Kiyosue K, Miwa Y. Kiyosue K, et al. Heliyon. 2020 Mar 11;6(3):e03504. doi: 10.1016/j.heliyon.2020.e03504. eCollection 2020 Mar. Heliyon. 2020. PMID: 32190754 Free PMC article.

References

1. J Mol Biol. 1967 Jun 14;26(2):365-9 - PubMed
1. J Virol. 1989 Jun;63(6):2644-9 - PubMed
1. Proc Natl Acad Sci U S A. 1974 Mar;71(3):631-3 - PubMed
1. J Mol Biol. 1976 Apr 15;102(3):511-30 - PubMed
1. Proc Natl Acad Sci U S A. 1982 Nov;79(22):6777-81 - PubMed

Multiple EBNA1-binding sites are required to form an EBNA1-dependent enhancer and to activate a minimal replicative origin within oriP of Epstein-Barr virus - PubMed (original) (raw)