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Chen L, Wang X, Fluck MM. Independent contributions of polyomavirus middle T and small T to the regulation of early and late gene expression and DNA replication. J Virol. 2006;80(15):7295-307doi: 10.1128/JVI.00679-06.
Chen, L., Wang, X., & Fluck, M. M. (2006). Independent contributions of polyomavirus middle T and small T to the regulation of early and late gene expression and DNA replication. Journal of virology, 80(15), 7295-307. https://doi.org/10.1128/JVI.00679-06
Chen, Li, et al. "Independent contributions of polyomavirus middle T and small T to the regulation of early and late gene expression and DNA replication." Journal of virology vol. 80,15 (2006): 7295-307. doi: https://doi.org/10.1128/JVI.00679-06
Chen L, Wang X, Fluck MM. Independent contributions of polyomavirus middle T and small T to the regulation of early and late gene expression and DNA replication. J Virol. 2006 Aug;80(15):7295-307. doi: 10.1128/JVI.00679-06. PMID: 16840310; PMCID: PMC1563708.
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J Virol. 2006 Aug;80(15):7295-307. doi: 10.1128/JVI.00679-06.

Independent contributions of polyomavirus middle T and small T to the regulation of early and late gene expression and DNA replication.

Journal of virology

Li Chen, Xiaoyu Wang, Michele M Fluck

Affiliations

  1. Department of Microbiology and Molecular Genetics, Interdepartmental Program in Cell and Molecular Biology, Michigan State University, East Lansing, MI 48824-1101, USA.

PMID: 16840310 PMCID: PMC1563708 DOI: 10.1128/JVI.00679-06

Abstract

We previously showed that murine polyomavirus mutants that lack both middle T (MT) and small T (ST) functions have a severe pleiotropic defect in early and late viral gene expression as well as genome amplification. The respective contribution of MT and ST to this phenotype was unclear. This work separates the roles of MT and ST in both permissive mouse cells and nonpermissive rat cells. It demonstrates for the first time a role for both proteins. To gain insight into the signaling pathways that might be required, we focused on MT and its mutants. The results show that each of the major MT signaling connections, Shc, phosphatidylinositol 3'-kinase, and phospholipase C gamma1, could contribute in an additive way. Unexpectedly, a mutant lacking all these connections because the three major tyrosines had been converted to phenylalanine retained some activity. A mutant in which all six MT C-terminal tyrosines had been mutated was inactive. This suggests a novel signaling pathway for MT that uses the minor tyrosines. What is common to ST and the individual MT signaling pathways is the ability to signal to the polyomavirus enhancer, in particular to the crucial AP-1 and PEA3/ets binding sites. This connection explains the pleiotropy of MT and ST effects on transcription and DNA replication.

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