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Recombinant avian oncoviruses. I. Alterations in the precursor to the internal structural proteins.
Authors:R Shaikh  M Linial  J Coffin  R Eisenman
Affiliation:1. Center for Cancer Research and Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 02138, USA;2. Department of Medicine, Division of Oncology, University of Washington School of Medicine, Seattle, Washington 98195, USA;3. Fred Hutchinson Cancer Research Center, Seattle, Washington 98104, USA;4. Tufts Medical School, Department of Molecular Biology and Microbiology, Boston, Massachusetts 02111, USA
Abstract:The synthesis of the gag precursor protein (Pr76) was studied in a number of recombinant avian oncoviruses, which were selected for recombination between the env and pol genes or the env and src genes. Such studies show that the electrophoretic mobility of the gag precursor protein of recombinant viruses (ΔPr76) was greater than that of the parental gene product (Pr76) in 16 of 24 cases. Viruses derived from recombination between endogenous (RAV-0) and exogenous viruses (RSV), as well as between two exogenous viruses, showed the ΔPr76 phenotype. In an mRNA-dependent rabbit reticulocyte translation system, 35 S RNA isolated from PR-RSV-C directed the synthesis of Pr76, while RNA isolated from a recombinant between PR-RSV-C and RAV-0 directed the synthesis of ΔPr76. These observations show that the synthesis of ΔPr76 is due to an alteration in the genome related to recombination. An analysis of the RNase T1-resistant oligonucleotides demonstrated a crossover near the 5′ end of the genome (which may be within the gag gene) in two recombinant virus clones which synthesize ΔPr76 in infected cells; but no crossover was detected near the 5′ end of the genome in a third recombinant virus clone which synthesizes Pr76 in infected cells. Our data suggest that the synthesis of ΔPr76 is a consequence of recombination near the 5′ end of the genome.
Keywords:To whom all requests for reprints and correspondence should be addressed: Center for Cancer Research   MIT   Cambridge   Massachusetts 02138.
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