Transcriptional Control by Retroviral LTR Regions
Murine leukemia viruses represent a polymorphic group of retroviruses. Individual isolates differ in species and tissue tropism and in their specificity and potency of pathogenic properties. Some viruses induce lymphomas with high incidence and a latency period of a few months when injected into newborn mice of various inbred strains, whereas others show a weaker and less specific pathogenicity. The pathogenic effects of these weaker viruses include various lymphomas and leukemias as well as neoplastic and non-neoplastic abnormalities in bone tissues. Recombination mapping between thymomagenic and weakly leukemogenic viruses has localized a major determinant of the oncogenic potency to the long terminal repeat (LTR) region of the viruses, (DesGroseillers et al., 1983; DesGroseiller and Jolicoeur, 1984; Lenz et al., 1984). Recombination mapping between viruses that yield thymic and erythroid leukemias has also localized the determinants for tissue specificity to the LTR region, (Chatis et al., 1983, 1984; Ishimoto et al., 1985; Vogt et al., 1985). The LTR regions contain sequences necessary for the initiation and termination of retroviral transcription including promotor elements, termination signals and enhancers. Mapping studies of the more potent MuLVs point to the transcriptional control region containing an enhancer structure as a disease determinant, (Chatis et al., 1984; Ishimoto et al., 1985; Bösze et al., 1986, (MoMuLV, Friend MuLv); Des Groseillers and Jolicoeur, 1984, (GrossA); Lenz et al., 1984; Celander and Haseltine, 1984, (SL3 - 3)).
KeywordsLong Terminal Repeat Murine Leukemia Virus Repeat Structure Chloramphenicol Acetyl Transferase Long Terminal Repeat Sequence
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