Werner Helicase Control of Human Papillomavirus 16 E1-E2 DNA Replication Is Regulated by SIRT1 Deacetylation

Author:

Das Dipon1,Bristol Molly L.1ORCID,Smith Nathan W.1,James Claire D.1,Wang Xu1,Pichierri Pietro2,Morgan Iain M.13

Affiliation:

1. Department of Oral and Craniofacial Molecular Biology, VCU Philips Institute for Oral Health Research, Virginia Commonwealth University School of Dentistry, Richmond, Virginia, USA

2. Department of Environment and Health, Istituto Superiore di Sanità, Rome, Italy

3. VCU Massey Cancer Center, Richmond, Virginia, USA

Abstract

HPV16 is the major viral human carcinogen responsible for between 3 and 4% of all cancers worldwide. Following infection, this virus activates the DNA damage response (DDR) to promote its life cycle and recruits DDR proteins to its replicating DNA in order to facilitate homologous recombination during replication. This promotes the production of viable viral progeny. Our understanding of how HPV16 replication interacts with the DDR remains incomplete. Here, we demonstrate that the cellular deacetylase SIRT1, which is a part of the E1-E2 replication complex, regulates recruitment of the DNA repair protein WRN to the replicating DNA. We demonstrate that WRN regulates the level and fidelity of E1-E2 replication. Overall, the results suggest a mechanism by which SIRT1 deacetylation of WRN promotes its interaction with E1-E2-replicating DNA to control the levels and fidelity of that replication.

Funder

HHS | NIH | National Cancer Institute

Publisher

American Society for Microbiology

Subject

Virology,Microbiology

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