Inhibition of host RNA polymerase II-dependent transcription by vesicular stomatitis virus results from inactivation of TFIID - PubMed (original) (raw)
. 1998 Nov 25;251(2):383-92.
doi: 10.1006/viro.1998.9413.
Affiliations
- PMID: 9837802
- DOI: 10.1006/viro.1998.9413
Free article
Inhibition of host RNA polymerase II-dependent transcription by vesicular stomatitis virus results from inactivation of TFIID
H Yuan et al. Virology. 1998.
Free article
Abstract
During infection with vesicular stomatitis virus (VSV), host-cell mRNA synthesis is inhibited due to shut off of host-cell transcription. The transcriptional activity of nuclear extracts prepared from VSV-infected cells was compared to the activity of nuclear extracts from uninfected cells. An exogenous DNA template was used which contained an adenovirus major late promoter (AdMLP) but lacked upstream activating sequences, so that only basal transcription activity was assayed in these experiments. AdMLP-initiated transcription was decreased by 75% in nuclear extracts from infected cells as early as 3 h p.i. and by >90% by 6 h p.i. Mixing nuclear extracts from uninfected and VSV-infected cells revealed that the inhibition was caused by lack of an active form of a host factor involved in basal transcription rather than by the presence of an excess of inhibitory factor. To determine which transcription factors were lacking from nuclear extracts of infected cells, host transcription initiation factors isolated from uninfected cells by ion-exchange chromatography were added separately to nuclear extracts inactivated by VSV infection. A phosphocellulose column fraction from uninfected cells eluted with 0. 8 M KCl, which contained transcription factor IID (TFIID), overcame the inhibition. The corresponding fraction from infected cells had no detectable activity in a TFIID-dependent in vitro transcription assay. TATA-binding protein (TBP) is the DNA-binding subunit of TFIID and has been shown previously to substitute for TFIID in basal transcription. Purified recombinant TBP also reconstituted the transcription activity of nuclear extracts from infected cells, supporting the idea that TFIID is the target of virus-induced inhibition. Western blot analysis showed that the level of TBP in nuclear extracts or in the 0.8 M KCl column fraction was not changed by VSV infection. These results indicated that VSV infection leads to an inhibition of host transcription by inactivation of TFIID rather than reduction in the level of TFIID.
Copyright 1998 Academic Press.
Similar articles
- Potency of wild-type and temperature-sensitive vesicular stomatitis virus matrix protein in the inhibition of host-directed gene expression.
Lyles DS, McKenzie MO, Ahmed M, Woolwine SC. Lyles DS, et al. Virology. 1996 Nov 1;225(1):172-80. doi: 10.1006/viro.1996.0585. Virology. 1996. PMID: 8918544 - Transcription factor TFIID recruits factor CPSF for formation of 3' end of mRNA.
Dantonel JC, Murthy KG, Manley JL, Tora L. Dantonel JC, et al. Nature. 1997 Sep 25;389(6649):399-402. doi: 10.1038/38763. Nature. 1997. PMID: 9311784 - Retinoid-dependent transcription: the RAR/RXR-TBP-EIA/EIA-LA connection.
Meyer M, Sonntag-Buck V, Keaveney M, Stunnenberg HG. Meyer M, et al. Biochem Soc Symp. 1996;62:97-109. Biochem Soc Symp. 1996. PMID: 8971343 Review. - Inhibition of cell functions by RNA-virus infections.
Kääriäinen L, Ranki M. Kääriäinen L, et al. Annu Rev Microbiol. 1984;38:91-109. doi: 10.1146/annurev.mi.38.100184.000515. Annu Rev Microbiol. 1984. PMID: 6093688 Review.
Cited by
- Understanding and altering cell tropism of vesicular stomatitis virus.
Hastie E, Cataldi M, Marriott I, Grdzelishvili VZ. Hastie E, et al. Virus Res. 2013 Sep;176(1-2):16-32. doi: 10.1016/j.virusres.2013.06.003. Epub 2013 Jun 22. Virus Res. 2013. PMID: 23796410 Free PMC article. Review. - Exploiting Bacterial Effector Proteins to Uncover Evolutionarily Conserved Antiviral Host Machinery.
Embry A, Baggett NS, Heisler DB, White A, de Jong MF, Kocsis BL, Tomchick DR, Alto NM, Gammon DB. Embry A, et al. bioRxiv [Preprint]. 2024 Jan 30:2024.01.29.577891. doi: 10.1101/2024.01.29.577891. bioRxiv. 2024. PMID: 38352400 Free PMC article. Updated. Preprint. - Contrasting effects of matrix protein on apoptosis in HeLa and BHK cells infected with vesicular stomatitis virus are due to inhibition of host gene expression.
Kopecky SA, Lyles DS. Kopecky SA, et al. J Virol. 2003 Apr;77(8):4658-69. doi: 10.1128/jvi.77.8.4658-4669.2003. J Virol. 2003. PMID: 12663772 Free PMC article. - Antitumor and antimetastatic activities of vesicular stomatitis virus matrix protein in a murine model of breast cancer.
Shi W, Tang Q, Chen X, Cheng P, Jiang P, Jing X, Chen X, Chen P, Wang Y, Wei Y, Wen Y. Shi W, et al. J Mol Med (Berl). 2009 May;87(5):493-506. doi: 10.1007/s00109-009-0444-5. Epub 2009 Mar 4. J Mol Med (Berl). 2009. PMID: 19259640 - Infectious hematopoietic necrosis virus matrix protein inhibits host-directed gene expression and induces morphological changes of apoptosis in cell cultures.
Chiou PP, Kim CH, Ormonde P, Leong JA. Chiou PP, et al. J Virol. 2000 Aug;74(16):7619-27. doi: 10.1128/jvi.74.16.7619-7627.2000. J Virol. 2000. PMID: 10906216 Free PMC article.