Localization of the Coding Region for a 35000 Dalton Polypeptide on the Genome of Herpes Simplex Virus Type 2

Suh, Martha; Chauvin, Christiane; Filion, Mario; Shore, Gordon C.; Frost, Éric

doi:10.1099/0022-1317-64-9-2079

Cited by 7 publications

(3 citation statements)

References 28 publications

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“…The results obtained from both studies demonstrated no significant mutagenic effect, thus failing to support the hit-and-run hypothesis. The mapping of the ribonucleotide reductase 36K subunit gene to the left portion of the BgllI N (Galloway et al, 1982;Preston et al, 1984;Suh et al, 1983) raised the possibility that transient or stable expression of 36K could participate in the induction of the transformed phenotype (Huszar & Bacchetti, 1983 -Garapin et al, 1981) and pXho3 (Suh et al, 1983). Several cell lines having resistance to G418 and the morphological changes commonly observed in transformed NIH 3T3 cells were selected and tested for the retention of the viral sequences.…”

Section: Retention and Expression Of The Left End Subfragment Of The mentioning

confidence: 99%

“…The immunoblots were probed with two different polyclonal antibodies (P9 and RS21) at a dilution of 1/500. P9 antiserum was raised against a synthetic peptide corresponding to the nine carboxy-terminal amino acids of the 36K protein (Cohen et al, 1986) and RS21 was raised against total HSV-2-infected cells (Suh et al, 1983). As shown in Fig.…”

Section: Retention and Expression Of The Left End Subfragment Of The mentioning

confidence: 99%

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Retention and Expression of the Left End Subfragment of the Herpes Simplex Virus Type 2 BglII N DNA Fragment Do Not Correlate with Tumorigenic Conversion of NIH 3T3 Cells

Kessous-Elbaz

Pelletier²,

Cohen³

et al. 1989

Journal of General Virology

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SUMMARYCotransfection experiments have been carried out using recombinant plasmids pAG60, conferring resistance to antibiotic G418, and pXho3 which contains the left end subfragment (map coordinates 0.583 to 0.596) of the transforming herpes simplex virus type 2 BglII N DNA fragment and encodes the 36K polypeptide associated with the viral ribonucleotide reductase activity. Several NIH 3T3 cell clones resistant to G418 and having morphological changes commonly observed for transformed NIH 3T3 cells were isolated and examined for the presence and stable retention of the viral sequences. Seven of the clones that retained the transfected viral sequences were analysed for the expression of the 36K polypeptide and the tumorigenic phenotype. The results gathered from these studies show that neither the retention of the viral DNA nor the expression of the 36K polypeptide correlated with tumorigenic conversion of these cells.

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Section: Retention and Expression Of The Left End Subfragment Of The mentioning

confidence: 99%

Section: Retention and Expression Of The Left End Subfragment Of The mentioning

confidence: 99%

Retention and Expression of the Left End Subfragment of the Herpes Simplex Virus Type 2 BglII N DNA Fragment Do Not Correlate with Tumorigenic Conversion of NIH 3T3 Cells

Kessous-Elbaz

Pelletier²,

Cohen³

et al. 1989

Journal of General Virology

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“…RNA for the 35K polypeptide is apparently synthesized in small amounts in the absence of DNA synthesis and probably corresponds to the abundant 37.8K protein reported by Docherty et al (4). Suh and coworkers (19) mapped the coding sequences for the 35K protein at ca. 0.585 to 0.596 map units and the coding sequences for the 56K protein at ca.…”

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confidence: 99%

Characterization of mRNAs that map in the BglII N fragment of the herpes simplex virus type 2 genome

Jenkins¹,

Howett²

1984

J Virol

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The BglIl N DNA fragment (0.580 to 0.620 map units) of herpes simplex virus type 2 strain (333) is of interest because of its transforming potential. This fragment contains either partial or the complete coding sequences for nine mRNA transcripts that can be detected during a lytic infection. Subclones of the BglII N DNA fragment were generated in plasmid vectors, and the approximate locations of the mRNA transcripts were mapped by RNA blot hybridization technology. Precise 5' or 3' ends (or both) of these mRNA species were determined by Si nuclease mapping, using the BglIl N subclones as DNA probes. At least four mRNA transcripts are fully * Corresponding author.

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Retention of herpes simplex virus type II sequences in bglII n-transformed cells after co-transfection with a selectable marker.

Saavedra¹,

Kessous-Elbaz²

1985

The EMBO Journal

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Transformation of mammalian cells by total u.v.‐inactivated herpes simplex virus II (HSVII) or cloned fragments thereof (BglII n, BglII C) has been complicated both by a low efficiency of oncogenic transformation and the disappearance of viral DNA and/or viral products initially detected in the transformed cell lines. In an attempt to effect a stable integration of BglII n and to elucidate the role of HSVII in oncogenic transformation, we have co‐transfected NIH 3T3 cells with pAG60, a plasmid which confers resistance to the G418 antibiotic, and plasmids containing either BglII n in its entirety (pNB2) or one of five subfragments of BglII n. Several isolated clones exhibit a transformed phenotype as expressed by rapid growth in low serum concentrations and colony formation in soft agar. We have obtained a markedly reduced frequency of biochemical transformants when co‐transfecting pNB2 in comparison with the numbers obtained when cotransfecting the five subfragments. Furthermore, a greater proportion of subfragment‐transfected colonies contain viral DNA, and in higher copy number, than observed in the pAG60/pNB2 clones. We have also found viral DNA to be more stably integrated in the subfragment‐transfected clones than in the pNB2‐transfected clones.

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Localization of the Coding Region for a 35000 Dalton Polypeptide on the Genome of Herpes Simplex Virus Type 2

Cited by 7 publications

References 28 publications

Retention and Expression of the Left End Subfragment of the Herpes Simplex Virus Type 2 BglII N DNA Fragment Do Not Correlate with Tumorigenic Conversion of NIH 3T3 Cells

Retention and Expression of the Left End Subfragment of the Herpes Simplex Virus Type 2 BglII N DNA Fragment Do Not Correlate with Tumorigenic Conversion of NIH 3T3 Cells

Characterization of mRNAs that map in the BglII N fragment of the herpes simplex virus type 2 genome

Retention of herpes simplex virus type II sequences in bglII n-transformed cells after co-transfection with a selectable marker.

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