Herpes simplex virus type I disrupts the ATR-dependent DNA-damage response during lytic infection.

Herpes simplex virus type I disrupts the ATR-dependent DNA-damage response during lytic infection. Research Abstract Details 

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Herpes simplex virus type I disrupts the ATR-dependent DNA-damage response during lytic infection. Abstract Text:

Dianna E Wilkinson,Sandra K Weller,

Like other DNA viruses, herpes simplex virus type 1 (HSV-1) interacts with components of the cellular response to DNA damage. For example, HSV-1 sequesters endogenous, uninduced, hyperphosphorylated RPA (replication protein A) away from viral replication compartments. RPA is a ssDNA-binding protein that signals genotoxic stress through the ATR (ataxia telangiectasia-mutated and Rad3-related) pathway. The sequestration of endogenous hyperphosphorylated RPA away from replicating viral DNA suggests that HSV-1 prevents the normal ATR-signaling response. In this study we examine the spatial distribution of endogenous hyperphosphorylated RPA with respect to ATR, its recruitment factor, ATRIP, and the cellular dsDNA break marker, gammaH2AX, during HSV-1 infection. The accumulation of these repair factors at DNA lesions has previously been identified as an early event in signaling genotoxic stress. We show that HSV-1 infection disrupts the ATR pathway by a mechanism that prevents the recruitment of repair factors, spatially uncouples ATRIP from ATR and sequesters ATRIP and endogenous hyperphosphorylated RPA within virus-induced nuclear domains containing molecular chaperones and components of the ubiquitin proteasome. The HSV-1 immediate early protein ICP0 is sufficient to induce the redistribution of ATRIP. This is the first report that a virus can disrupt the usually tight colocalization of ATR and ATRIP.

Herpes simplex virus type I disrupts the ATR-dependent DNA-damage response during lytic infection. Publishing Authors By Initials

DE Wilkinson,SK Weller,

For similar cells: cells, cultured: cell line: vero cells research abstracts see: cells: cells, cultured: cell line: vero cells research

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Herpes simplex virus type I disrupts the ATR-dependent DNA-damage response during lytic infection. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: Journal of cell science

VOLUME: 119

Page Numbers: 2695-703

Journal Abbreviation: J. Cell. Sci.

ISSN: 0021-9533

DAY: 6

MONTH: 06

YEAR: 2006

Herpes simplex virus type I disrupts the ATR-dependent DNA-damage response during lytic infection. Information

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LANGUAGE: eng

NlmUniqueID: 52457

Herpes simplex virus type I disrupts the ATR-dependent DNA-damage response during lytic infection. Keywords Mesh Terms:

KEYWORDS: Vero Cells

MESH TERMS: metabolism

Chemical & Substance for Abstract: Herpes simplex virus type I disrupts the ATR-dependent DNA-damage response during lytic infection. Information

Substance Name: Vmw110 protein, Human herpesvirus 1

Registry Number: EC 6.3.2.19

Grant and Affiliation Information for Herpes simplex virus type I disrupts the ATR-dependent DNA-damage response during lytic infection.

AFFILIATION: Department of Molecular, Microbial and Structural Biology MC3205, University of Connecticut Health Center, 263 Farmington Avenue, Farmington, CT 06030, USA.

Country: England

AGENCY: United States NIAID

GRANT: F32 AI054042

ACRONYM: AI

MEDLINETA: J Cell Sci

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