Selectivity in Integration Sites of Adenoviral DNA

Doerfler, Walter; Stabel, Silvia; Ibelgaufts, Horst; Sutter, Delphine De; Neumann, Rainer; Groneberg, Jürgen; Scheidtmann, Karl Heinz; Deuring, Renate; Winterhoff, Ute

doi:10.1101/sqb.1980.044.01.057

Cited by 40 publications

(44 citation statements)

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“…In the present report we confirm that the major portion of the integrated Adl2 DNA sequences is inserted into the host genome as the entire DNA molecule (9,10) and demonstrate that the integrated Adl2 DNA sequences in the HA12/7, T637, A2497-2, and A2497-3 lines are extensively methylated.…”

supporting

confidence: 82%

“…The patterns of integration of Adl2 DNA sequences in four lines of Adl2-transformed hamster cells (9,10) and four lines of Adl2-induced rat brain tumor cells (10,11) have been analyzed in detail. During the analysis of the DNA from Adl2-transformed hamster cells it was noted that Hpa II (5'-C-C-G-G-3') and Smn I (5'-C-C-C-G-G-G-3') did not effectively cleave integrated Adl2 DNA sequences, whereas EcoRI, BamHI, and Bgl II cleaved integrated viral DNA as efficiently as control virion DNA.…”

mentioning

confidence: 99%

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Methylation of integrated adenovirus type 12 DNA sequences in transformed cells is inversely correlated with viral gene expression.

Sutter¹,

Doerfler²

1980

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

284

124

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The adenovirus type 12 (Adl2) DNA sequences integrated into the DNA of four lines of Adl2-transformed hamster cells are extensively methylated. Methylation in mammalian cell DNA is believed to occur predominantly at 5'-C-G-3' sequences. The majority, although not all, of the 5'-C-C-G-G-3 sequences present in integrated Adl2 DNA are methylated. Ad12 DNA isolated from purified virions, on the other hand, is not methylated to any significant extent.

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supporting

confidence: 82%

mentioning

confidence: 99%

Methylation of integrated adenovirus type 12 DNA sequences in transformed cells is inversely correlated with viral gene expression.

Sutter¹,

Doerfler²

1980

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

284

124

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“…This event would probably demand some measure of host sequence specificity to SV40 integration in anchorage-transformed, 100K T antigen-containing mouse cells. Earlier studies on mouse cells have argued against such host specificity (6, 33), although partial transformants of adenovirus type 2 do make proteins which are of hybrid virus-host origin (14,30).…”

Section: Methodsmentioning

confidence: 99%

Nonlytic simian virus 40-specific 100K phosphoprotein is associated with anchorage-independent growth in simian virus 40-transformed and revertant mouse cell lines.

Chen¹,

Verderame²,

Lo³

et al. 1981

Mol. Cell. Biol.

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Normal fibroblasts display two distinct growth controls which can be assayed as requirements for serum or for anchorage. Interaction of mouse 3T3 fibroblasts with simian virus 40 (SV40) thus generates four classes of transformed cells. We have examined viral gene expression in these four classes of cell lines. Immunoprecipitation of [3S]methionine-labeled cell extracts with an antiserum obtained from tumor-bearing hamsters detected the SV40 large T and small t proteins (94,000 molecular weight [94K], 17K) and the nonviral host 54K protein in all cell lines tested. A tumor antigen with an apparent molecular weight of 100,000 was also found in some, but not all, lines. Similar "super T" molecules have been found by others in many rodent transformed lines. We carried out an analysis of the relation of phenotype to relative amounts of these proteins in cell lines of the four classes, using the Spearman rank correlation test. The amount of the 100K T antigen relative to the 94K T antigen or to total viral protein was well correlated with the ability to form colonies in semisolid medium. No significant correlation was found between quantities of labeled 94K T antigen, 54K host antigen, or 17K t antigen and either serum or anchorage independence. Mouse cells transformed with the small t SV40 deletion mutant 884 synthesized a 100K T antigen, suggesting that small t is not required for the production of this protein. The 100K T antigen migrated more slowly than lytic T. Since mixtures of extracts from cells expressing and lacking the 100K T antigen yielded the expected amount of this protein, it is unlikely that the 100K T derives from the 94K protein by a posttranslational modification.

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“…The small number of copies of integrated SA7 DNA fragments in the genome of transformed or tumour cells, as well as the absence of a portion of the SA7 genome in tumour cells suggests that the integration of the highly oncogenic adenovirus SA7 DNA into the cell genome is similar to that of the non-oncogenic human adenoviruses of group C. Doerfler et al (1980) suggested that the difference in DNA persistence patterns between Adl 2-transformed cells and Ad2-and Ad5-transformed cells may be explained by differences in permissiveness, It has been reported that rat cells are semi-permissive for Ad2 (Gallimore, 1974) and that hamster cells are totally non-permissive for Adl2 (Fanning & Doerfler, 1976). The hypothesis of Doerfler et al (1980) is that in a semi-permissive system there is a strong selective force directed against the persistence of entire Ad2 and Ad5 genome in the cell, since subsequent replication of the viral genome might kill the cell.…”

mentioning

confidence: 99%

“…The hypothesis of Doerfler et al (1980) is that in a semi-permissive system there is a strong selective force directed against the persistence of entire Ad2 and Ad5 genome in the cell, since subsequent replication of the viral genome might kill the cell. In Ad 12-infected rodent cells, on the other hand, persistence and integration of the intact viral DNA will not necessarily have a deleterious effect on cell survival.…”

mentioning

confidence: 99%

Analysis of Sequences of Simian Adenovirus SA7 (C8) DNA in Transformed Rat Cells and Hamster Tumour Cells

Gartel

Chaplygina

Ponomareva

et al. 1983

Journal of General Virology

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SUMMARYDifferent methods of molecular hybridization were used to study DNA sequences of the highly oncogenic simian adenovirus SA7 (C8) present in the genomes of two transformed rat cell lines and in cells from three hamster tumours induced by adenovirus SA7. The entire DNA or the left-hand terminal SalI C fragment (19-5 ~ of the genome) were employed. All cell lines retained an intact left-hand region of the SA7 genome (0 to 12-4 map units). The blot hybridization technique failed to detect any site specificity of integration of SA7 DNA into the cell genome. In all cell lines the expression of the BglII D fragment (1.8 to l0 map units) of SA7 DNA was observed. As judged by the patterns of integration of virus sequences into the cell genome, the highly oncogenic simian adenovirus SA7 (C8) is similar to the non-oncogenic human adenoviruses of group C, and is different from the highly oncogenic human adenovirus type 12.

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Selectivity in Integration Sites of Adenoviral DNA

Cited by 40 publications

References 0 publications

Methylation of integrated adenovirus type 12 DNA sequences in transformed cells is inversely correlated with viral gene expression.

Methylation of integrated adenovirus type 12 DNA sequences in transformed cells is inversely correlated with viral gene expression.

Nonlytic simian virus 40-specific 100K phosphoprotein is associated with anchorage-independent growth in simian virus 40-transformed and revertant mouse cell lines.

Analysis of Sequences of Simian Adenovirus SA7 (C8) DNA in Transformed Rat Cells and Hamster Tumour Cells

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