Alterations in the genomes of avian sarcoma viruses

Mason, William S.; Linial, Maxine L.; Hsu, T W; Eisenman, Robert N.; Townsend, J B; Mark, George E.; Seal, Geeta; Aldrich, Carol E.; Taylor, John M.

doi:10.1016/0042-6822(82)90484-6

Cited by 8 publications

(3 citation statements)

References 41 publications

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“…The 62 000-dalton a subunit, derived from the amino terminus of the 92 000-dalton 0 polypeptide, contains DNA polymerase and RNase H activities whose functions appear distinct in viral DNA synthesis (Gerard & Grandgenett, 1980). A nonconditional RSV mutant isolated from RSV-transformed quail cells and containing a large deletion in the carboxyl terminus of the polymerase gene produces noninfectious virus particles and encodes a gag-pol polyprotein containing only a subunit but not pp32 determinants (Mason et al, 1979(Mason et al, , 1982.…”

Section: Discussionmentioning

confidence: 99%

Avian retrovirus pp32 DNA binding protein. Preferential binding to the promoter region of long terminal repeat DNA

Knaus¹,

Hippenmeyer²,

Misra³

et al. 1984

Biochemistry

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The avian retrovirus pp32 protein possesses DNA endonuclease activity and unique DNA binding properties. An improved purification procedure was developed for pp32, resulting in a severalfold increase in the yield of this virion protein. By use of the nitrocellulose filter binding assay, the protein retains approximately 2-fold more supercoiled (form I) DNA molecules than equivalent linear duplex DNA molecules. Single-stranded DNA is only slightly preferred over double-stranded DNA for pp32 binding. The pp32 DNA binding sites on form I pBR322 DNA which contained an insert of avian retrovirus long terminal repeat (LTR) DNA were determined. A preformed protein-DNA complex was digested with one of several different multicut restriction enzymes and filtered through nitrocellulose filters. Fragments containing viral LTR DNA sequences and plasmid DNA containing promoter sequences for the ampicillin and tetracycline genes, sequences for the "left-end" inverted repeat of transposon 3, and sequences encompassing the carboxyl terminus of the beta-lactamase gene were preferentially retained on the filter by pp32. Partial mapping of pp32 DNA binding sites on LTR DNA was accomplished by generation of deletions in LTR DNA sequences. The pp32 protein preferentially bound viral DNA fragments which contain the viral promoter (TATTTAA) and the adjacent "R" repeat sequences. Computer analysis revealed that three of the four plasmid DNA fragments retained by pp32 contained LTR DNA promoter-like sequences (one mismatch only) which were part of statistically significant and thermodynamically stable hairpin structures.

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Section: Discussionmentioning

confidence: 99%

Avian retrovirus pp32 DNA binding protein. Preferential binding to the promoter region of long terminal repeat DNA

Knaus¹,

Hippenmeyer²,

Misra³

et al. 1984

Biochemistry

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“…It has been found that nondefective RSV segregated defective mutants at a relatively high frequency (10 to 15% of the total virus population) during the replication cycle (13,19). Therefore, some of these defective proviruses, particularly proviruses of the third type, may be formed from TK15 in a similar way.…”

Section: Figmentioning

confidence: 99%

Characterization of a Rous sarcoma virus mutant defective in packaging its own genomic RNA: biochemical properties of mutant TK15 and mutant-induced transformants

Koyama¹,

Harada²,

Kawai³

1984

J Virol

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The accompanying paper (S. Kawai and T. Koyama, J. Virol. 51:147-153, 1984) describes the isolation and biological properties of a mutant, TK15, derived from a Rous sarcoma virus mutant, tsNY68. The cisacting defect of the mutant is analyzed biochemically in this paper. TK15 virions released from virus-producing 15c(+) cells were deficient in viral genomic 39S RNA, although comparable amounts of viral RNAs were transcribed in 15c(+) and tsNY68-infected cells. Analysis of provirus DNA occurring in 15c(+) cells suggested that the mutant genome had a deletion of ca. 250 bases near the 5' end of the genome somewhere between the primer binding site and the 5' end of the gag-coding region. These findings indicate that at least part of the sequence lost in the TK15 genome is indispensable for packaging viral genomic RNA into virions. TK15 induces nonvirus-producing 15c(-) transformants at high frequency. Southern blot analysis of DNAs from those 15c(-) clone cells revealed that TK15-derived proviruses contained various extents of internal deletions. Many 15c(-) clones had a provirus carrying only the src gene with long terminal repeat sequences at both ends. The mechanism for the segregation of 15c(-) cells is discussed.

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“…The provirus integrated in RSV-transformed avian and mammalian cell lines is often altered to different degrees Hughes et al, 1978;Mason et al, 1979Mason et al, , 1982Boettiger, 1979. 1980], Alterations might have occurred even in freshly cloned viral stocks employed for infection, or in the course of cell transformation, by imperfec tions during the processes of reverse tran scription or integration, or altered proviruses might arise by reverse transcription of viral mRNA (see section IX).…”

Section: Structure Of Provirusmentioning

confidence: 99%

Rous Sarcoma Virus

Svoboda¹

1986

Intervirology

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Alterations in the genomes of avian sarcoma viruses

Cited by 8 publications

References 41 publications

Avian retrovirus pp32 DNA binding protein. Preferential binding to the promoter region of long terminal repeat DNA

Avian retrovirus pp32 DNA binding protein. Preferential binding to the promoter region of long terminal repeat DNA

Characterization of a Rous sarcoma virus mutant defective in packaging its own genomic RNA: biochemical properties of mutant TK15 and mutant-induced transformants

Rous Sarcoma Virus

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