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Modifications of both selectivity factor and upstream binding factor contribute to poliovirus-mediated inhibition of RNA polymerase I transcription

¹ Department of Microbiology, Immunology and Molecular Genetics, University of California Los Angeles, UCLA School of Medicine, 10833 Le Conte Avenue, Los Angeles, CA 90095, USA
² Department of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA

Correspondence
Asim Dasgupta
dasgupta{at}ucla.edu

Soon after infection, poliovirus (PV) shuts off host-cell transcription, which is catalysed by all three cellular RNA polymerases. rRNA constitutes more than 50 % of all cellular RNA and is transcribed from rDNA by RNA polymerase I (pol I). Here, evidence has been provided suggesting that both pol I transcription factors, SL-1 (selectivity factor) and UBF (upstream binding factor), are modified and inactivated in PV-infected cells. The viral protease 3C^pro appeared to cleave the TATA-binding protein-associated factor 110 (TAF₁₁₀), a subunit of the SL-1 complex, into four fragments in vitro. In vitro protease-cleavage assays using various mutants of TAF₁₁₀ and purified 3C^pro indicated that the Q²⁶⁵G²⁶⁶ and Q⁸⁰⁵G⁸⁰⁶ sites were cleaved by 3C^pro. Both SL-1 and UBF were depleted in PV-infected cells and their disappearance correlated with pol I transcription inhibition. rRNA synthesis from a template containing a human pol I promoter demonstrated that both SL-1 and UBF were necessary to restore pol I transcription fully in PV-infected cell extracts. These results suggested that both SL-1 and UBF are transcriptionally inactivated in PV-infected HeLa cells.

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