Literature DB >> 7941331

Genetic and biochemical evidence that EBNA 2 interaction with a 63-kDa cellular GTG-binding protein is essential for B lymphocyte growth transformation by EBV.

R Yalamanchili1, X Tong, S Grossman, E Johannsen, G Mosialos, E Kieff.   

Abstract

Epstein-Barr virus (EBV) nuclear protein 2 (EBNA 2) is an acidic transcriptional transactivator of virus and cell gene expression and is essential for growth transformation of primary B lymphocytes. EBNA 2 transactivation of response elements (E2REs) can be mediated by interaction with a GTGGGAA-specific DNA-binding factor(s). We now purify the factor by S-Sepharose and EBNA 2 affinity chromatography and identify it as a single 63-kDa protein. The protein is shown to specifically coimmunoprecipitate with EBNA 2 from lymphoblasts transfected with an EBNA 2 FLAG expression vector. Mutation of GTG to TCT in a GTGGGAA motif common to the Cp, LMP2, and LMP1 promoters results in loss of recognition by p63. EBNA 2 amino acids 310-336 are sufficient for p63 binding. The only motif in this 27 amino acid sequence which is common to the EBNA 2 genes of EBV types 1 and 2 is GPPWWPP (I/V) (C/R) DP, which is therefore likely to mediate p63 interaction. Mutation of WW to SS or FF ablates interaction with p63, indicating that both the hydrophobic and aromatic characteristics of WW are essential for its "key" interaction with p63. EBNA 2 with a WW mutated to SS is also unable to marker rescue primary B lymphocyte transforming virus from cells infected with an EBNA 2-deleted virus, while otherwise isogenic wild-type EBNA 2 readily marker rescues transforming virus in parallel experiments. EBNA 2 transactivation through the Cp E2RE is completely abolished by the WW to SS mutation while transactivation of -234 to +40 LMP1 E2RE is only partially affected. These genetic and biochemical experiments support the hypothesis that EBNA 2 WW interaction with a p63 GTGGGAA-binding protein is essential for EBV-mediated cell growth transformation because it specifically associates EBNA 2 with its response elements. This enables the EBNA 2 acidic domain to transcriptionally transactivate specific genes.

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Year:  1994        PMID: 7941331     DOI: 10.1006/viro.1994.1578

Source DB:  PubMed          Journal:  Virology        ISSN: 0042-6822            Impact factor:   3.616


  52 in total

1.  A role for SKIP in EBNA2 activation of CBF1-repressed promoters.

Authors:  S Zhou; M Fujimuro; J J Hsieh; L Chen; S D Hayward
Journal:  J Virol       Date:  2000-02       Impact factor: 5.103

2.  Intracellular forms of human NOTCH1 functionally activate essential Epstein-Barr virus major latent promoters in the Burkitt's lymphoma BJAB cell line but repress these promoters in Jurkat cells.

Authors:  M Cotter; J Callahan; J Aster; E Robertson
Journal:  J Virol       Date:  2000-02       Impact factor: 5.103

Review 3.  The genetic approach to the Epstein-Barr virus: from basic virology to gene therapy.

Authors:  H J Delecluse; W Hammerschmidt
Journal:  Mol Pathol       Date:  2000-10

4.  Modulation of histone acetyltransferase activity through interaction of epstein-barr nuclear antigen 3C with prothymosin alpha.

Authors:  M A Cotter; E S Robertson
Journal:  Mol Cell Biol       Date:  2000-08       Impact factor: 4.272

5.  Conserved region CR2 of Epstein-Barr virus nuclear antigen leader protein is a multifunctional domain that mediates self-association as well as nuclear localization and nuclear matrix association.

Authors:  Michiko Tanaka; Akihiko Yokoyama; Mie Igarashi; Go Matsuda; Kentaro Kato; Mikiko Kanamori; Kanji Hirai; Yasushi Kawaguchi; Yuji Yamanashi
Journal:  J Virol       Date:  2002-02       Impact factor: 5.103

6.  Epstein-Barr virus nuclear protein 2 has at least two N-terminal domains that mediate self-association.

Authors:  S Harada; R Yalamanchili; E Kieff
Journal:  J Virol       Date:  2001-03       Impact factor: 5.103

7.  Regulation of the Epstein-Barr virus C promoter by AUF1 and the cyclic AMP/protein kinase A signaling pathway.

Authors:  E M Fuentes-Pananá; R Peng; G Brewer; J Tan; P D Ling
Journal:  J Virol       Date:  2000-09       Impact factor: 5.103

8.  EBV nuclear antigen EBNALP dismisses transcription repressors NCoR and RBPJ from enhancers and EBNA2 increases NCoR-deficient RBPJ DNA binding.

Authors:  Daniel Portal; Bo Zhao; Michael A Calderwood; Thomas Sommermann; Eric Johannsen; Elliott Kieff
Journal:  Proc Natl Acad Sci U S A       Date:  2011-04-25       Impact factor: 11.205

9.  Sequence and functional analysis of EBNA-LP and EBNA2 proteins from nonhuman primate lymphocryptoviruses.

Authors:  R Peng; A V Gordadze; E M Fuentes Pananá; F Wang; J Zong; G S Hayward; J Tan; P D Ling
Journal:  J Virol       Date:  2000-01       Impact factor: 5.103

10.  Epstein-barr virus-induced changes in B-lymphocyte gene expression.

Authors:  Kara L Carter; Ellen Cahir-McFarland; Elliott Kieff
Journal:  J Virol       Date:  2002-10       Impact factor: 5.103

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