Inhibition of Rous sarcoma virus by α-amanitin: Possible role of cell DNA-dependent RNA polymerase form II

Dinowitz, Marshall

doi:10.1016/0042-6822(75)90174-9

Cited by 28 publications

(10 citation statements)

References 29 publications

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“…ASV RNA is thought, however, to be synthesized by RNA polymerase 11 (32,33). The sequence G-G-(X)5-A-A-A-A-G, located between positions 293 and 282, has been found in at least two instances at the presumed promoter sites for recognition by RNA polymerase II (34,35).…”

Section: Resultsmentioning

confidence: 99%

Unusual features in the nucleotide sequence of a cDNA clone derived from the common region of avian sarcoma virus messenger RNA.

Yamamoto¹,

Jay²,

Pastan³

1980

Proc. Natl. Acad. Sci. U.S.A.

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We have constructed a recombinant plasmid containing a 700-base pair (bp) cDNA copy of the common region present at the 3' end of Schmidt-Ruppin avian sarcoma virus (ASV) 21S mRNA. The cDNA was inserted into plasmid pBR322 at the Pst I site by the G-C tailing method. A restriction map of the cloned insert from a recombinant plasmid pSR1 indicates that it corresponds to the 3' end of the ASV genome. R-loop analysis with ASV genomic RNA indicates that the insert is colinear with the ASV genome over most of its length. The sequence of 331 bp at the 3' end of the DNA insert was determined and shows that the insert contains extra sequences not found at the 3' end of ASV genomic RNA. Following the terminally redundant sequence of 20 bp that has been found at the extreme 3' end of genomic RNA is a sequence of 79 bp that is almost identical to that located immediately next to the 20-bp repeat at the 5' end of ASV genomic RNA. This is followed by 18 bp of unique sequence, possibly of host origin. The structure of the clone suggests that ASV mRNA may differ from genomic RNA at its 3' end and that 21S mRNA is transcribed from integrated ASV DNA and contains at its 3' end sequences derived both from the 5' end of the ASV genome and from host DNA adjacent to the site of integration. The presence of termination codons in all three reading frames suggests that the common region probably does not contain coding sequences. However, the presence of sequences that resemble probable promoter sites supports the possibility that this region may be involved in the regulation of transcription.

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Section: Resultsmentioning

confidence: 99%

Unusual features in the nucleotide sequence of a cDNA clone derived from the common region of avian sarcoma virus messenger RNA.

Yamamoto¹,

Jay²,

Pastan³

1980

Proc. Natl. Acad. Sci. U.S.A.

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“…Viral RNA is synthesized from integrated DNA provirus by cellular RNA polymerase II as judged by the sensitivity of this reaction to a-amanitin (Rymo et al, 1974;Weissmann et al, 1975;Dinowitz, 1975). The initiation of viral RNA synthesis shows a requirement for mitosis Temin, 1972, 1974).…”

Section: A Synopsis Of Rna Tumor Virus Infectionmentioning

confidence: 98%

Genetics of RNA Tumor Viruses

Vogt

1977

Regulation and Genetics

105

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“…The form I is resist.ant and form I I I is several hundred-fold to 1000-fold less sensitive to ~-amanitin t h a n is the form I I polymerase (20,27,28,31). The sensitivity of R S V synthesis in vivo to inhibition b y small amounts of ~.-amanitin indicates t h a t the form I I polymerase is required for RSV transcription (9). W i t h i n a few hours of exposure of RSV transformed cells to e-amanitin, the synthesis of R S V declines but continues a t a reduced level for several more hours (9).…”

Section: Introductionmentioning

confidence: 99%

“…The sensitivity of R S V synthesis in vivo to inhibition b y small amounts of ~.-amanitin indicates t h a t the form I I polymerase is required for RSV transcription (9). W i t h i n a few hours of exposure of RSV transformed cells to e-amanitin, the synthesis of R S V declines but continues a t a reduced level for several more hours (9). The continued synthesis of RSV after prolonged exposure of the cells to the toxin suggested the possibility that.…”

Section: Introductionmentioning

confidence: 99%

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Altered sensitivity of Rous sarcoma virus transformed cells to inhibition of RNA synthesis by ?-amanitin

Dinowitz

Lindell²,

O'Malley³

1977

Archives of Virology

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Chick embryo cells transformed by Rous sarcoma virus (RSV) continue to synthesize 40--50 percent of control amounts of RNA following 12--24 hour exposure to 2 microng/ml of the toxin whereas normal chick embryo cells similarly treated synthesize less than 5 percent of control amounts of RNA. Analysis of cells treated with alpha-amanitin, or the resistant forms I and III polymerase, do not increase in infected cells over the levels found in uninfected control cells during the first 24 hours following infection indicating that increase in polymerase levels in infected cells does not account for the observed resistance. No significant difference was detected in the sensitivity to alpha-amanitin in the form II polymerase isolated from normal and transformed cells; The greater sensitivity of normal cells to alpha-amanitin can be reduced by growing the cells at low cell density but the resistance of RSV transformed cells is not significantly altered by changes in cell density. The results suggest that the resistance of RSV transformed cells may be related to altered control of density dependent contact-inhibition of the transformed cells.

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Inhibition of Rous sarcoma virus by α-amanitin: Possible role of cell DNA-dependent RNA polymerase form II

Cited by 28 publications

References 29 publications

Unusual features in the nucleotide sequence of a cDNA clone derived from the common region of avian sarcoma virus messenger RNA.

Unusual features in the nucleotide sequence of a cDNA clone derived from the common region of avian sarcoma virus messenger RNA.

Genetics of RNA Tumor Viruses

Altered sensitivity of Rous sarcoma virus transformed cells to inhibition of RNA synthesis by ?-amanitin

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