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S Manteuil-Brutlag

Publications and source records attributed to S Manteuil-Brutlag.

4 recordsLinked to original sources
PubMed1980

Radiation leukemia virus contains two distinct viral RNAs.

We have analyzed the RNA genome of RadLV/VL3, a highly oncogenic murine leukemia virus. This virus is produced by a permanent cell line derived from a radiation leukemia virus-induced thymic lymphoma of C57BL/Ka mice. Two distinct RNA components were found in the virions: a 70S dimer containing two 8 kb RNA subunits and a 54S dimer containing two 5.6 kb RNAs. A nononcogenic retrovirus, BL/Ka(B), endogenous in the same strain of mice, contains only 8 kb viral RNA subunits. The linkages between both RadLV/VL3 dimers have identical thermal stabilities. Both dimers can serve as primer templates for reverse transcriptase and both produce very similar "strong-stop" cDNAs 147 +/- 1 bases long. Sequences at the 5' end of the 5.6 kb subunit contain the genes for the viral proteins p15 and p12, but the gene for p30 is either absent or partially deleted. In vitro translation of the 5.6 kb RNA yields a 100,000 molecular weight protein containing antigenic determinants which react with antibody to p15 but not with antibody to p30. In addition, cells producing RadLV/VL3 virus synthesize a novel of 1.6 kb poly(A)-containing cytoplasmic RNA which shows very little if any homology with BL/Ka(B) viral sequences.

Base Sequence↗
PubMed1977

Physical and genetic characterization of deletion mutants of simian virus 40 constructed in vitro.

Mutants of simian virus 40 (SV40), with deletions ranging in size from fewer than 3 to 750 base pairs located throughout the SV40 genome, were obtained by infecting CV-1P cells with linear SV40 DNA and DNA of an appropriate helper virus. The linear DNA was obtained by complete cleavage of closed circular DNA with Hae II or Bam HI endonuclease or partial cleavage with either Hae III endonuclease or nuclease S1, followed, in some cases, by mild digestion with phage lambda 5' -exonuclease. The following mutants with deletions in the late region of the SV40 genome were obtained and characterized. Ten, containing deletions at the Hae II endonuclease site (map location 0.83), define a new genetic complementation group, E, grow extremely slowly without helper virus, and cause alterations only in VP2. Two mutants with deletions in the region 0.92 to 0.945 affect both VP2 and VP3, demonstrating that VP3 shares sequences with the C-terminal portion of VP2. The mutant with a deletion at 0.93 is the first deletion mutant in the D complementation group and is also temperature sensitive; the mutant with a deletion at 0.94 is viable and grows normally. Three mutants with deletions at the EcoRI endonuclease site (0/1.0) and eleven with deletions at the BamHI endonuclease site (0.15) fall into the B/C complementation group. Six additional mutants with deletions at the BamHI endonuclease site are viable, growing more slowly than wild type. VP1 is the only polypeptide affected by mutants in the B/C group. A mutant with a deletion of the region 0.72 to 0.80 has a polar effect, failing to express the E, D, and B/C genes. Mutants with deletions in the early region (0.67 counterclockwise to 0.17) at 0.66 to 0.59, 0.48, 0.47, 0.33, and 0.285 to 0.205 are all members of the A complementation group. Thus, the A gene is the only viral gene in the early region whose expression is necessary for productive infection of permissive cells. Since mutants with deletions in the region 0.59 to 0.54 are viable, two separate regions are essential for expression of the gene A function: 0.66 to 0.59 and 0.54 to 0.21. Mutants with deletions at 0.21 and 0.18 are viable. Approximate map locations of SV40 genes and possible models for their regulation are discussed.

Cell Line↗
PubMed1975

[The "sarc" gene].

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Alpharetrovirus↗