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Published May 1981 | Published
Journal Article Open

Genome structure of Abelson murine leukemia virus variants: proviruses in fibroblasts and lymphoid cells

Abstract

We have prepared full-length DNA clones of the Abelson murine leukemia virus (A-MuLV) genome. A specific probe homologous to the central portion of the A-MuLV genome was prepared by nick translation of a subcloned restriction fraction from the cloned DNA. The probe was used to examine the genome structure of several A-MuLV variants. The conclusions are: (i) three viruses coding for Abelson-specific proteins of molecular weight 120,000, 100,000, and 90,000 had genomes indistinguishable in size, suggesting that the shorter proteins are the result of early translational termination; (ii) compared with the genome encoding the 120,000-dalton (120K) protein, a genome coding for a 160K protein was 0.8 kilobase larger in the A-MuLV-specific region; and (iii) a genome coding for a 92K protein had a 700-base pair deletion internal to the coding region. This mutant was transformation defective: its 92K protein lacked the protein kinase activity normally associated with the A-MuLV protein, and cells containing the virus were not morphologically transformed. In addition, we determined the number of A-MuLV proviruses in each of several transformed fibroblast and lymphoid cells prepared by infection in vitro. These experiments show that a single copy of the A-MuLV provirus is sufficient to transform both types of cells and that nonproducer cells generally have only one integrated provirus.

Additional Information

© 1981 American Society for Microbiology. Received 25 November 1980a; Accepted 30 January 1981. This work was supported by Public Health Service grant CA-24220 (to N.R.), program project grant CA-24530 (to N.R.), grant CA-26717 (to D.B.), and grant CA-14051 (core grant to S. E. Luria), all from the National Cancer Institute. S.P.G. was a postdoctoral fellow of the Jane Coffin Childs Memorial Fund for Medical Research. O.N.W. was a postdoctoral fellow of the Helen Hay Whitney Foundation. N.R. is a recipient of a Research Scholar Award from the American Cancer Society (Massachusetts division). D.B. is an American Cancer Society research Professor.

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August 19, 2023
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