Molecular mechanisms involved in morphological variation of avian sarcoma virus-infected rat cells

Chiswell, David J.; Enrietto, Paula J.; Evans, Siân; Quade, Kristina; Wyke, John A.

doi:10.1016/0042-6822(82)90137-4

Cited by 38 publications

(39 citation statements)

References 27 publications

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“…Two sub-clones (i.e., 13N and 21N) have lost the transformed phenotype and contain no detectable viral transcripts (Chiswell et al, 1982). When these 'flat revertants' are treated with the antimetabolite, aza-cytidine (aza-C), and recloned, transformed colonies containing viral transcripts emerge at a high frequency (D.J.Chiswell and J.A.Wyke, in preparation).…”

Section: Integrated Polyoma Sequencesmentioning

confidence: 99%

“…One mouse line transformed by polyoma (i.e., Tsa 3T3) was also included (Lania et al, , 1980. All express a transformed phenotype and contain high concentrations of viral transcripts (Chiswell et al, 1982;Kamen et al, 1979). As a control we mapped the unexpressed albumin gene.…”

Section: Introductionmentioning

confidence: 99%

“…taining viral sequences integrated at one different cellular site, were obtained by transformation of Rat-I cells (Mishra and Ryan, 1973) with polyoma (Lania et al, , 1980 or ASV (Wyke and Quade, 1980;Chiswell et al, 1982;Varmus et al, 1981). One mouse line transformed by polyoma (i.e., Tsa 3T3) was also included (Lania et al, , 1980.…”

Section: Introductionmentioning

confidence: 99%

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Active viral genes in transformed cells lie close to the nuclear cage.

Cook¹,

Lang²,

Hayday³

et al. 1982

The EMBO Journal

108

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Nuclear DNA is looped by attachment to a matrix or cage. Using nine different lines transformed by polyoma or avian sarcoma virus, we have mapped viral sequences integrated within these loops. In all lines that contain high concentrations of viral transcripts and express the transformed phenotype, the integrated viral genes lie close to the points of attachment to the cage. Integration of polyoma DNA induces outlying cellular sequences to become closely associated with the cage. The strength of this correlation between gene activity and proximity to the cage was examined using sub‐clones of one avian sarcoma virus transformant. Proviral sequences are closely associated with the cage in this transformant, much less so in two untransformed ‘flat revertants’ which contain no detectable viral transcripts but regain their close association with the cage in two retransformed derivatives.

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Section: Integrated Polyoma Sequencesmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Active viral genes in transformed cells lie close to the nuclear cage.

Cook¹,

Lang²,

Hayday³

et al. 1982

The EMBO Journal

108

View full text Add to dashboard Cite

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“…There are several reports on cellular control of the process of ASV replication: Neiman et al (1978) reported that ASV DNA could not be integrated normally into chicken lymphoid cells; Deng et al (1974) and other authors (Deng et al, 1977;Quintrell et al, 1980;Chiswell et al, 1982) reported that mammalian cells modulated the expression of integrated ASV genomes by regulating the production of viral mRNA. We have also reported that CEF produced avian sarcoma viruses as efficiently as td viruses, but that DEF produced sarcoma viruses less efficiently than td viruses early after infection at low m.o.i.…”

Section: Discussionmentioning

confidence: 99%

Isolation and Characterization of Host Range Mutants of Avian Sarcoma Virus

Shimakage

Yutsudo

Hakura

et al. 1983

Journal of General Virology

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SUMMARYTwo host range mutants of avian sarcoma virus (ASV) were isolated from a clone of the Bratislava 77 strain, subgroup C (B77-C). An HR-mutant was obtained by adaptation to duck cells and showed almost the same efficiencies of transformation (e.o.t.) and growth in cultures of chick embryo fibroblasts (CEF) and duck embryo fibroblasts (DEF). An HR + mutant showed lower e.o.t, and slower growth on DEF than on CEF. Characterization of these mutants and wild-type B77-C showed that (i) unlike the host range mutants reported previously, these mutants and wild-type B77-C have common antigenicity, (ii) the number of infective centres is almost the same for the two mutants and the wild-type, and so the adsorption and integration of these viruses are similar, and (iii) the content of viral RNA in DEF infected with HR-is increased and decreased in the case of HR + compared with the wild-type.

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“…The transformed cell line designated All, subclone 'VIT', was cloned and established as a stable line with its transformation phenotype characterised by morphology, growth in agar, stable insertion of complete provirus into the host genome, proviral RNA transcripts and proviral src gene expression (Chiswell et al, 1982 DNase I inhibition assay for actin Actin in monomeric and polymeric form was assayed in the cells using the DNase 1 inhibition assay essentially as described by Blikstad et al (1978) with minor modifications. A DNA substrate solution of 80mg 1-1 DNA (Sigma) in 0.1 M tris HCI buffer, pH 7.5 and containing 4mM MgSO4 and 1.8 mM CaCl2 was prepared, filtered through a Whatman No.…”

Section: Cellsmentioning

confidence: 99%

Effect of transformation by Rous sarcoma virus on the character and distribution of actin in Rat-1 fibroblasts: A biochemical and microscopical study

Holme¹,

Kellie²,

Wyke³

et al. 1986

Br J Cancer

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Actin has been measured in subcellular fractions from Rat-1 fibroblasts and in Rous sarcoma virus-transformed Rat-1 cells (VIT), using the DNase 1 inhibition assay. The transformed cells showed a significant shift in the actin monomer (G)in equilibrium with polymer (F) equilibrium within the cell cytosol, and a significant increase in actin in the Triton-insoluble cytoskeletal core in comparison with untransformed cells. This incorporation of actin into the cytoskeletal core fraction is associated with a change in filamentous actin assemblies from 'stress fibre' patterns to punctate filament aggregates. These differences have been correlated with changes in morphology, in actin, vinculin and alpha-actinin distribution, in adhesion plaque formation and with the production of pp60v-src-associated protein kinase activity in the transformed cells. Changes in actin distribution and its polymerization in response to src-gene expression may play an important role in the determination of the transformed cell characteristics. Images Figure 1 Figure 2 p471-a Figure 3 Figure 4 Figure 5

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Molecular mechanisms involved in morphological variation of avian sarcoma virus-infected rat cells

Cited by 38 publications

References 27 publications

Active viral genes in transformed cells lie close to the nuclear cage.

Active viral genes in transformed cells lie close to the nuclear cage.

Isolation and Characterization of Host Range Mutants of Avian Sarcoma Virus

Effect of transformation by Rous sarcoma virus on the character and distribution of actin in Rat-1 fibroblasts: A biochemical and microscopical study

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