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Journal of Virology, July 2008, p. 6409-6418, Vol. 82, No. 13
0022-538X/08/$08.00+0     doi:10.1128/JVI.00490-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Nuclear Marginalization of Host Cell Chromatin Associated with Expansion of Two Discrete Virus-Induced Subnuclear Compartments during Baculovirus Infection{triangledown}

Toshihiro Nagamine,* Yu Kawasaki,{dagger} Atsushi Abe, and Shogo Matsumoto

RIKEN Discovery Research Institute, Wako-shi, Saitama 351-0198, Japan

Received 5 March 2008/ Accepted 10 April 2008

Chromatin structure is strictly regulated during the cell cycle. DNA viruses occasionally disturb the spatial organization of the host cell chromatin due to formation of the viral DNA replication compartment. To examine chromatin behavior in baculovirus-infected cells, we constructed recombinant plasmids expressing fluorescent protein-tagged histone H4 molecules and visualized the intracellular localization of chromatin by their transient expression in live infected cells. Similar to other DNA viruses, the baculovirus Bombyx mori nucleopolyhedrovirus induced marginal relocation of chromatin within the nuclei of BmN cells, simultaneously with expansion of the viral DNA replication compartment, the virogenic stroma (VS). In the late stage of infection, however, the peristromal region (PR), another virus-induced subnuclear compartment, was also excluded from the chromatin-localizing area. Provided that late-gene products such as PR proteins (e.g., envelope proteins of the occlusion-derived virus) were expressed, blockage of viral DNA synthesis failed to inhibit chromatin relocation, despite abrogation of VS expansion. Instead, chromatin became marginalized concomitantly with PR expansion, suggesting that the PR contributes directly to chromatin replacement. In addition, chromatin was excluded from relatively large subnuclear structures that were induced in uninfected cells by cotransfection with four baculovirus genes, ie1, lef3, p143, and hr. Omission of any of the four genes, however, failed to result in formation of the large structures or chromatin exclusion. This correlation between compartmentalization and chromatin exclusion suggests the possibility that a chromatin-exclusive property of viral molecules, at least in part, supports nuclear compartmentalization of virus-infected cells.


* Corresponding author. Mailing address: Laboratory of Molecular Entomology, RIKEN, 2-1 Hirosawa, Wako-shi, Saitama 351-0198, Japan. Phone: 81-48-467-9584. Fax: 81-48-462-4678. E-mail: tnaga{at}riken.jp

{triangledown} Published ahead of print on 23 April 2008.

{dagger} Present address: Ebara Jitsugyo Co., Ltd., Central R&D Laboratory, 2-3-10 Kuriki, Asao-ku, Kawasaki 215-0033, Japan.


Journal of Virology, July 2008, p. 6409-6418, Vol. 82, No. 13
0022-538X/08/$08.00+0     doi:10.1128/JVI.00490-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.