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Journal of Virology, November 2002, p. 11123-11127, Vol. 76, No. 21
0022-538X/02/$04.00+0 DOI: 10.1128/JVI.76.21.11123-11127.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.
Daniela Mainz,
Ruud Mans,
Andreas Kremer,|| and Dagmar Knebel-Mörsdorf*
Max-Planck-Institute for Neurological Research and Department of Neurology, University of Cologne, D-50931 Cologne, Germany
Received 15 May 2002/ Accepted 17 July 2002
During the infection cycle of Autographa californica multicapsid nuclear polyhedrosis virus, the TATA-binding protein (TBP) of the insect host cell likely participates in early viral transcription, which is mediated by the host RNA polymerase II. However, the role of TBP in late and very late viral transcription, which is accomplished by an alpha-amanitin-resistant RNA polymerase, is unclear. We observed a dramatic increase of TBP protein during the late phases of infection. TBP mRNA levels, however, were not coordinately increased. Indirect-immunofluorescence studies revealed a nuclear redistribution of TBP during infection. After labeling of viral replication centers with bromodeoxyuridine (BrdU), costaining of TBP and BrdU showed that TBP localized to viral DNA replication centers. These results suggest a putative role of TBP during late viral transcription, which may occur in close proximity to viral DNA replication.
Present address: Institute of Molecular Virology, GSF, Neuherberg, Germany.
Present address: Department of Radiooncology, University of Tübingen, Tübingen, Germany.
Present address: Ordina Public West Nederland BV, Zoetermeer, The Netherlands.
|| Present address: LION Bioscience, Heidelberg, Germany.
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