Abstract
Enhanced expression of the cKi-ras proto-oncogene in a bone marrow-derived mouse cell line, 416B, has been shown to be associated with the integration of Friend viral DNA into the cellular gene. Here we report the results of experiments designed to clarify the molecular mechanism responsible for the cKi-ras overexpression. Based on primer extension analyses and DNA sequencing of cKi-ras cDNA clones, we have obtained evidence that the 416B cells contain viral-host chimaeric transcripts that initiate within the 3' long terminal repeat (LTR) of the integrated provirus. Processing of the transcripts from the rearranged cKi-ras gene includes an unexpected splicing event associated with the fortuitous creation of a cryptic donor splice site at the junction between the proviral and cellular DNA sequences. These data demonstrate that enhanced cKi-ras expression in the 416B cells results from a retroviral promoter insertion mechanism of transcriptional activation.
MeSH Terms
Animals
Base Sequence
Bone Marrow
Cell Line
DNA Transposable Elements
Exons
Female
Friend murine leukemia virus/genetics
Gene Expression Regulation, Neoplastic
Genes, ras
Mice
Mice, Inbred Strains
Molecular Sequence Data
Oligonucleotide Probes
Promoter Regions, Genetic
Proto-Oncogene Mas
Transcriptional Activation
Chemicals
DNA Transposable Elements
MAS1 protein, human
Oligonucleotide Probes
Proto-Oncogene Mas
Authors & Affiliations
3 authors, click to expand affiliations / ORCID
Trusko S P
Department of Human Genetics, University of Pennsylvania School of Medicine, Philadelphia 19104-6072.
Hoffman E K
George D L
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