The v-rel oncogene encodes a cell-specific transcriptional activator of certain promoters

C. Gelinas, H. M. Temin

Research output: Contribution to journalArticle

55 Citations (Scopus)

Abstract

Transformation by the v-rel oncogene of avian reticuloendotheliosis virus strain T (Rev-T) is primarily cell-specific. While v-rel efficiently transforms chicken spleen and bone marrow stem cells in vitro and induces rapid lethal lymphomas in young birds, it does not rapidly transform chicken embryo fibroblasts. The nuclear localization of the v-rel gene product in non-transformed fibroblasts along with its ability to function as a transforming protein in the nucleus of chicken spleen cells suggests that p59(v-rel) might belong to the family of nuclear oncoproteins and thus may express an immortalizing function in fibroblasts. To gain insight into the specificity of cell transformation by the v-rel oncogene, we determined whether v-rel could immortalize primary rat fibroblasts. Our experiments have shown that, unlike other nuclear oncoproteins, p59(v-rel) did not immortalize primary rat embryo fibroblasts. However p59(v-rel) was able to cooperate in a synergistic way with the polyomavirus middle T protein in inducing efficient transformation of established rat fibroblasts by increasing the steady-state level of middle T RNA, indicating that p59(v-rel) might function as a transactivator. Co-transfection of cells from different species with the v-rel gene along with constructs expressing the chloramphenicol acetyl transferase gene under the control of different promoters revealed that p59(v-rel) is a cell-specific transcriptional transactivator of certain promoters. Moreover, the extent of cell-specific transactivation by v-rel correlated with its toxic effect in these same cells.

Original languageEnglish (US)
Pages (from-to)349-355
Number of pages7
JournalOncogene
Volume3
Issue number4
StatePublished - Jan 1 1988
Externally publishedYes

Fingerprint

rel Genes
Fibroblasts
Chickens
Trans-Activators
Oncogene Proteins
Avian Reticuloendotheliosis Viruses
Spleen
Embryonic Structures
Polyomavirus Transforming Antigens
Aptitude
Poisons
Chloramphenicol
Transferases
Nuclear Family
Bone Marrow Cells
Transcriptional Activation
Birds
Transfection
Lymphoma
Stem Cells

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Genetics
  • Cancer Research

Cite this

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abstract = "Transformation by the v-rel oncogene of avian reticuloendotheliosis virus strain T (Rev-T) is primarily cell-specific. While v-rel efficiently transforms chicken spleen and bone marrow stem cells in vitro and induces rapid lethal lymphomas in young birds, it does not rapidly transform chicken embryo fibroblasts. The nuclear localization of the v-rel gene product in non-transformed fibroblasts along with its ability to function as a transforming protein in the nucleus of chicken spleen cells suggests that p59(v-rel) might belong to the family of nuclear oncoproteins and thus may express an immortalizing function in fibroblasts. To gain insight into the specificity of cell transformation by the v-rel oncogene, we determined whether v-rel could immortalize primary rat fibroblasts. Our experiments have shown that, unlike other nuclear oncoproteins, p59(v-rel) did not immortalize primary rat embryo fibroblasts. However p59(v-rel) was able to cooperate in a synergistic way with the polyomavirus middle T protein in inducing efficient transformation of established rat fibroblasts by increasing the steady-state level of middle T RNA, indicating that p59(v-rel) might function as a transactivator. Co-transfection of cells from different species with the v-rel gene along with constructs expressing the chloramphenicol acetyl transferase gene under the control of different promoters revealed that p59(v-rel) is a cell-specific transcriptional transactivator of certain promoters. Moreover, the extent of cell-specific transactivation by v-rel correlated with its toxic effect in these same cells.",
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The v-rel oncogene encodes a cell-specific transcriptional activator of certain promoters. / Gelinas, C.; Temin, H. M.

In: Oncogene, Vol. 3, No. 4, 01.01.1988, p. 349-355.

Research output: Contribution to journalArticle

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