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Journal of Virology, July 2003, p. 8087-8098, Vol. 77, No. 14
0022-538X/03/$08.00+0 DOI: 10.1128/JVI.77.14.8087-8098.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.
Terry Roberts,2 Deborah A. Trott,2,
Robert F. Newbold,2 and David A. Ornelles1*
Department of Microbiology and Immunology, Wake Forest University School of Medicine, Wake Forest University, Winston-Salem, North Carolina 27157-1064,1 The Brunel Institute of Cancer Genetics and Pharmacogenomics, Brunel University, Uxbridge, Middlesex UB8 3PH, United Kingdom2
Received 13 September 2002/ Accepted 22 April 2003
The adenovirus E1B-55K and E4orf6 proteins cooperate during virus infection while performing several tasks that contribute to a productive infection, including the selective nucleocytoplasmic transport of late viral mRNA. Previous studies have shown that the E4orf6 protein retains the E1B-55K protein in the nucleus of human and monkey cells, but not in those of rodents, suggesting that primate-specific cellular factors contribute to the E4orf6-mediated retention of the E1B-55K protein in the nucleus. In an effort to identify these proposed primate-specific cellular factors, the interaction of the E1B-55K and E4orf6 proteins was studied in a panel of stable human-rodent monochromosomal somatic cell hybrids. Analysis of this panel of cell lines has demonstrated the existence of an activity associated with human chromosome 21 that permits the E1B-55K and E4orf6 proteins to colocalize in the nucleus of a rodent cell. Additional hybrid cells bearing portions of human chromosome 21 were used to map this activity to a 10-megabase-pair segment of the chromosome, extending from 21q22.12 to a region near the q terminus. Strikingly, this region also facilitates the expression of adenovirus late genes in a rodent cell background while having little impact on the expression of early viral genes.
Present address: Department of Microbiology and Immunology, University of Michigan School of Medicine, Ann Arbor, MI 48109.
Present address: MRC Clinical Sciences Centre, Imperial College, London, United Kingdom.
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