Abstract
The transcriptional enhancers of retroviruses that lack an oncogene are important determinants of their oncogenicity. However, no specific cellular transcriptional activator has yet been found to determine the oncogenicity for any of these viruses. The SL3-3 enhancer factor 1 (SEF1) cellular transcriptional activators are expressed preferentially in T lymphocytes. In the SL3-3 murine leukemia virus enhancer, two different sequences can bind SEF1 activators. We show that mutation of the SEF1 binding sites disrupts the disease potential of SL3-3 murine leukemia virus, implying that SEF1 transcriptional activators are required for tumor induction by SL3-3. The SEF1 site mutations did not appear to affect the pathogenicity of SL3-3 by impairment of virus multiplication, but rather by a specific defect in the ability of neoplastic transformation.
MeSH Terms
Animals
Animals, Newborn
Base Sequence
Binding Sites
Cell Transformation, Neoplastic
DNA, Viral/analysis
Enhancer Elements, Genetic
Leukemia Virus, Murine/genetics,growth & development,physiology
Lymphoma/etiology
Mice
Molecular Sequence Data
Mutagenesis, Insertional
Mutagenesis, Site-Directed
Plasmids
Polymerase Chain Reaction
Precursor Cell Lymphoblastic Leukemia-Lymphoma/microbiology
Proviruses/genetics,physiology
Repetitive Sequences, Nucleic Acid
Trans-Activators/physiology
Transcription, Genetic
Chemicals
DNA, Viral
Trans-Activators
Authors & Affiliations
5 authors, click to expand affiliations / ORCID
Hallberg B
Department of Applied Cell and Molecular Biology, University of Umeå, Sweden.
Schmidt J
Luz A
Pedersen F S
Grundström T
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