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J. Virol. doi:10.1128/JVI.02021-07
Copyright (c) 2008, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

The Role of Cellular Phosphatase cdc25C in Herpes Simplex Virus 1 replication

Marjorie B. Kovler Viral Oncology Laboratories, The University of Chicago, 910 East 58th Street, Chicago, Illinois 60637

^* To whom correspondence should be addressed. Email: bernard.roizman{at}bsd.uchicago.edu.

	Abstract

Earlier studies have shown that in herpes simplex virus 1 - infected cells ICP22 upregulates the accumulation of a subset of ₂ proteins exemplified by the products of U_L38, U_L41, and U_S11 genes. The ICP22-dependent process involves degradation of cyclins A and B1, the stabilization and activation of cdc2, physical interaction of activated cdc2 with the U_L42 DNA synthesis processivity factor, and recruitment and phosphorylation of topoisomerase II by the cdc2/U_L42 complex. Activation of cdc2, the first step in the process, is a key function of the mitotic phosphatase cdc25C. To define the role of cdc25C, we probed some features of the ICP22 dependent pathway of upregulation of ₂ genes in cdc25C^-/- and in cdc25C^+/+ cells derived from sibling mice. We report that in infected cells lacking cdc25C the cyclin B1 turned over at a slower rate, that cdc2 increased in amount and that U_S11 and U_L38 proteins and infectious virus accumulated in smaller amounts than in wild-type infected cells. The reduction in U_L38 protein accumulation and virus was greater in cdc25C^-/- cells infected with ICP22 minus virus than in cells infected with wild-type virus. We conclude that cdc25C phosphatase plays a role in viral replication and that this role extends beyond its function of activating cdc2 for initiation of the ICP22-dependent cascade for upregulation of ₂ gene expression.

This article has been cited by other articles:

• Smith-Donald, B. A., Roizman, B. (2008). The Interaction of Herpes Simplex Virus 1 Regulatory Protein ICP22 with the cdc25C Phosphatase Is Enabled In Vitro by Viral Protein Kinases US3 and UL13. J. Virol. 82: 4533-4543 [Abstract] [Full Text]