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At least 271 records · Page 15Linked to original sources
PubMed1975

Infectious DNA from cells infected with Rous sarcoma virus, reticuloendotheliosis virus or Rous-associated virus-O.

We have described an efficient and quantitative assay for infectious DNA of the avian ribodeoxyviruses and have applied this method to study the possible existence of infectious viral DNAs in uninfected cells. Infectious DNA from cells infected with RSV or REV consisted of a single unit of DNA with a specific infectivity of 10(-5)-10(-6). The minimum molecular weight of RSV DNA required for infection of chicken cells was about 6 million, while the minimum molecular weight of infectious REV DNA was about 20 million. This difference may reflect complementation of the RSV DNA by endogenous avian leukosis virus-related DNA in uninfected chicken cells. Uninfected chicken cells do not contain infectious DNA for an REV, nor for a strongly transforming or a nontransforming avian leukosis virus.

Animals↗
PubMed1976

Genomic complexities of murine leukemia and sarcoma, reticuloendotheliosis, and visna viruses.

The genetic complexities of several ribodeoxyviruses were measured by quantitative analysis of unique RNase T1-resistant oligonucleotides from 60-70S viral RNAs. Moloney murine leukemia virus was found to have an RNA complexity of 3.5 x 10(6) daltons, whereas Moloney murine sarcoma virus had a significantly smaller genome size of 2.3 x 10(6). Reticuleondotheliosis and visna virus RNAs had complexities of 3.9 x 10(6), respectively. Analysis of RNase A-resistant oligonucleotides of Rous sarcoma virus RNA gave a complexity of 3.6 x 10(6), similar to that previously obtained with RNase T1-resistant oligonucleotides. Since each of these viruses was found to have a unique sequence genomic complexity near the molecular weight of a single 30-40S viral RNA subunit, it was concluded that ribodeoxyvirus genomes are at least largely polyploid.

Base Sequence↗
PubMed1988

Functional interaction between transcriptional elements in the long terminal repeat of reticuloendotheliosis virus: cooperative DNA binding of promoter- and enhancer-specific factors.

Transcription from reticuloenodotheliosis virus strain T (REV-T), an avian retrovirus unrelated to avian leukosis and sarcoma viruses, is modulated by sequences in at least five functional domains. A promoter containing a TATA and multiple CCAAT motifs in U3 of the long terminal repeat was absolutely required for transcription. Transcriptional efficiency was greatly augmented by an enhancer immediately upstream, which contained a 22-base-pair repeated sequence. Transcription was further influenced by a negative-acting domain in the 5' region of U3 and two downstream domains in the transcribed non-protein-coding region. One of these latter domains contained a consensus enhancer core sequence and positively affected transcription in both mammalian and avian cells; the other acted negatively in a dog cell line. Transcription from REV-T in vivo required cellular factors which could be competed for specifically by the promoter or enhancer domain. The downstream domains competed with reporter genes containing these domains, but not directly with the U3 sequences. The promoter, enhancer, and the positive-acting downstream domains formed multiple complexes with distinct classes of cellular factors in both avian and mammalian cell extracts. Binding of factors to the promoter and enhancer domains was cooperative when these domains were joined in cis.

Animals↗