NDLI: Nuclear retention of ICP0 in cells exposed to HDAC inhibitor or transfected with DNA before infection with herpes simplex virus 1

Content Provider	PubMed Central
Author	Maria, Kalamvoki Roizman, Bernard
Abstract	The α (immediate early) protein ICP0 of herpes simplex virus 1 enhances the expression of genes introduced by infection or transfection. Early in infection it performs two key functions: It blocks the silencing of the viral DNA by cellular proteins and it blocks the IFN stimulated host response to infection. Between 5 and 9 h after infection, ICP0 is translocated to the cytoplasm but remains dynamically associated with proteasomes. In this report we show that in permissive cells that are poor expressors of transfected genes (HEp-2, U2OS, etc.), ICP0 is retained in the nucleus if the cells had been transfected with DNA and then infected. The retention is DNA dose- and size-dependent but not DNA type-dependent. Retention of ICP0 is also a consequence of infection with wild-type virus concomitant with exposure of cells to sodium butyrate. ICP0 is not retained in transfected/infected cells that efficiently express transfected genes (HEK293, rabbit skin cells). The retention of ICP0 in the nucleus is concordant with failure to degrade PML and disperse ND10 structures, and delays in the transition to post α genes expression, translocation of components of the CoREST/REST/HDAC1 complex and histone relocation in the infected cell. The data suggest that (i) retention of ICP0 is linked to its function to remodel acetylated DNA but not DNA in heterochromatin. This function is independent of response elements embedded in the DNA and (ii) transfection-resistant cells do take up DNA but process it differently than cells that readily express transfected genes.
Related Links	http://dx.doi.org/10.1073/pnas.0810879105
Ending Page	20493
Page Count	6
Starting Page	20488
File Format	PDF
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	51
Volume Number	105
Language	English
Publisher	National Academy of Sciences
Publisher Date	2008-12-23
Access Restriction	Open
Rights Holder	National Academy of Sciences
Subject Keyword	General Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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