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Published on: February 22, 2015
R7, a spontaneous mutant of Moloney murine sarcoma virus 124 with three direct repeats and an in-frame truncated
1Department of Carcinogenesis, The University of Texas M.D. Anderson Cancer Center, Science Park, Smithville, Texas 78957, USA.
Abstract:
We have isolated Recombinant 7 (R7), a spontaneous mutant of SV7, a molecular clone of MoMuSV124. Like SV7, R7 induces subcutaneous fibrosarcomas, spleen tumors, and mesentery tumors infiltrated by proliferating vessels lined by transformed endothelial cells. However, it also induces brain lesions. We have molecularly cloned and sequenced the R7 proviral DNA and shown that the R7 genome consists of 3401 bp. It has three direct repeats in each enhancer. Its coding sequence consists of only 176 bp of p15, 263 bp of p30, a 7-bp insertion, and 853 bp of an N-terminally truncated mos gene. From the sequence of R7 we have deduced that the truncated mos sequence is in-frame with all of the gag sequence and the 7-bp insertion. The incorporation of the 3' end of the p15 sequence further suggests that the R7 Gag-Mos is myristylated. We have also shown that the molecularly cloned R7 virus transformed NIH/3T3 fibroblasts about sevenfold better than the parental SV7. We have also confirmed that molecularly cloned R7 induces the same disease phenotype as that induced by the nonmolecularly cloned R7.
Insights
Recombinant 7 (R7), a mutant of MoMuSV124, induces tumors and brain lesions. Its unique genetic makeup enhances NIH/3T3 fibroblast transformation, offering insights into viral oncogenesis.
Area of Science:
- Oncology
- Virology
- Molecular Biology
Background:
- Murine osteosarcoma virus (MoMuSV124) is a retrovirus known to cause tumors.
- SV7 is a molecular clone of MoMuSV124 that induces various tumors.
- Recombinant 7 (R7) is a spontaneous mutant of SV7 with altered oncogenic properties.
Purpose of the Study:
- To characterize the genetic makeup and oncogenic potential of Recombinant 7 (R7).
- To compare the transforming ability of R7 with its parental virus, SV7.
- To investigate the molecular basis for R7's distinct disease phenotype.
Main Methods:
- Molecular cloning and sequencing of the R7 proviral DNA.
- Analysis of the R7 genome for structural and coding sequences.
- Transformation assays using NIH/3T3 fibroblasts.
Main Results:
- R7 genome is 3401 bp, featuring direct repeats in enhancers and a unique coding sequence.
- R7 contains truncated gag and mos genes, with a 7-bp insertion and p15 sequence, suggesting myristylation of R7 Gag-Mos.
- Molecularly cloned R7 exhibited a sevenfold higher transformation efficiency of NIH/3T3 fibroblasts compared to SV7.
- R7 induces subcutaneous fibrosarcomas, spleen tumors, mesentery tumors, and brain lesions, consistent with its parental virus but with added neuropathology.
Conclusions:
- R7 possesses a distinct genetic structure that enhances its transforming ability.
- The genetic alterations in R7 contribute to its specific oncogenic profile, including brain lesions.
- R7 serves as a valuable model for studying retroviral oncogenesis and the role of specific viral gene products.
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