Impact of the interaction between adenovirus E1A and CtBP on host cell gene expression
- PMID: 15899534
- DOI: 10.1016/j.virusres.2005.04.015
Impact of the interaction between adenovirus E1A and CtBP on host cell gene expression
Abstract
In cell lines harbouring inducible adenovirus E1A genes, the cytotoxicity of wild type E1A was manifested by poor and subsiding expression of the E1A protein during prolonged induction. In contrast, cells expressing E1A deleted in the C-terminal binding protein (CtBP)-interaction domain (E1ADeltaCID) demonstrated high levels of expression for extended time. Microarray analyses of host cell gene expression demonstrated that approximately 70% of the regulated genes were increased upon E1A induction and that the majority of E1A-regulated genes were similarly regulated by wild type E1A and E1ADeltaCID. However, for 29 genes, regulation by wild type E1A and E1ADeltaCID were different. Consistent with the altered transforming capacity of E1A unable to bind CtBP, genes involved in tumour cell progression and growth suppression were found among the differently regulated genes. Moreover, promoter sequences of genes up regulated by wild type E1A and/or repressed by E1ADeltaCID demonstrated a higher prevalence of potential binding sites for the CtBP-targeted transcription factors Ets, Ikaros and/or partial differentialEF1/ZEB, suggesting that the failure to block CtBP-repression contributed to the "hyper-transforming" phenotype of E1ADeltaCID. Since E1ADeltaCID also specifically activated host cell gene expression, we find it likely that additional, possibly CtBP-independent, mechanisms contribute to the altered phenotype of E1ADeltaCID-expressing cells.
Similar articles
-
Functional knockout of the corepressor CtBP by the second exon of adenovirus E1a relieves repression of transcription.Exp Cell Res. 2001 Aug 15;268(2):284-93. doi: 10.1006/excr.2001.5280. Exp Cell Res. 2001. PMID: 11478854
-
Structural determinants in adenovirus 12 E1A involved in the interaction with C-terminal binding protein 1.Virology. 2000 Nov 10;277(1):156-66. doi: 10.1006/viro.2000.0580. Virology. 2000. PMID: 11062046
-
Gene expression profiling by DNA microarray analysis in mouse embryonic fibroblasts transformed by rasV12 mutated protein and the E1A oncogene.Mol Cancer. 2003 Mar 19;2:19. doi: 10.1186/1476-4598-2-19. Mol Cancer. 2003. PMID: 12685932 Free PMC article.
-
Modulation of oncogenic transformation by the human adenovirus E1A C-terminal region.Curr Top Microbiol Immunol. 2004;273:139-61. doi: 10.1007/978-3-662-05599-1_5. Curr Top Microbiol Immunol. 2004. PMID: 14674601 Review.
-
Recent lessons in gene expression, cell cycle control, and cell biology from adenovirus.Oncogene. 2005 Nov 21;24(52):7673-85. doi: 10.1038/sj.onc.1209040. Oncogene. 2005. PMID: 16299528 Review.
Cited by
-
C-Terminal Binding Protein: Regulator between Viral Infection and Tumorigenesis.Viruses. 2024 Jun 19;16(6):988. doi: 10.3390/v16060988. Viruses. 2024. PMID: 38932279 Free PMC article. Review.
-
Subversion of CtBP1-controlled macropinocytosis by human adenovirus serotype 3.EMBO J. 2008 Apr 9;27(7):956-69. doi: 10.1038/emboj.2008.38. Epub 2008 Mar 6. EMBO J. 2008. PMID: 18323776 Free PMC article.
-
Multiple ASF/SF2 sites in the human papillomavirus type 16 (HPV-16) E4-coding region promote splicing to the most commonly used 3'-splice site on the HPV-16 genome.J Virol. 2010 Aug;84(16):8219-30. doi: 10.1128/JVI.00462-10. Epub 2010 Jun 2. J Virol. 2010. PMID: 20519389 Free PMC article.
-
HPV-16 E2 contributes to induction of HPV-16 late gene expression by inhibiting early polyadenylation.EMBO J. 2012 May 22;31(14):3212-27. doi: 10.1038/emboj.2012.147. EMBO J. 2012. PMID: 22617423 Free PMC article.
-
Polypyrimidine tract binding protein induces human papillomavirus type 16 late gene expression by interfering with splicing inhibitory elements at the major late 5' splice site, SD3632.J Virol. 2008 Apr;82(7):3665-78. doi: 10.1128/JVI.02140-07. Epub 2008 Jan 23. J Virol. 2008. PMID: 18216120 Free PMC article.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources