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The U3 long terminal repeat (LTR) region of the avian retroviruses has been extensively characterized as a model of a strong transcription regulatory unit.This compact enhancer and promoter drives high levels of viral and cellular gene transcription in many cell types in birds and in mammals.Viral mRNA and genomic RNA transcripts can comprise up to 20% of the total RNA in infected cells (Varmus and Swanstrom, 1984).The high level expression of the retroviral LTR has been exploited in the development of reporter gene expression vectors (Gorman eta/., 1982) and of expression vectors for mammalian gene therapy studies (Yoshimura et a/., t992).Infectious avian retroviral constructs have also been engineered for gene expression studies (Garber eta/., 1991; Hughes eta/., 1987) and for development of transgenic chickens (Salter et al., 1987).Analysis of this potent transcription regulatory unit will provide insight to the molecular basis for enhancer and promoter function and will help in the design of improved retroviral vectors.The avian retroviral LTR is also of interest because of its essential role in oncogenesis.The Rous sarcoma virus carries a transduced v-src oncogene and rapidly induces fibrosarcoma in chickens, caused by deregulated LTR-driven v-src expression (Bishop and Varmus, 1984).Related strains of viruses carry other oncogenes such as v-fps or v-ms.
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Alanna Ruddell (1995) studied this question.
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