Activation of mutated simian virus 40 enhancers by amplification of wild-type enhancer elements.
AUTOR(ES)
Clarke, J
RESUMO
We show that duplication of any one of three separate simian virus 40 enhancer elements, A, B, or C, can compensate for loss of function in the remaining two. Simian virus 40 revertants containing point mutations within the A and C (dpm16) or B and C (dpm26) enhancer elements contain tandem duplications that include the remaining wild-type element. These simple tandem duplications can create enhancers 25-fold more active than that of the parental mutant. These revertants can arise by illegitimate recombination between heterologous viral genomes. This was demonstrated by the recombinants resulting from a mixed infection with the viruses dpm16 and dpm2, which contain mutations in the A and C elements and the B element, respectively.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=255952Documentos Relacionados
- Analysis of simian virus 40 wild-type and mutant virions by agarose gel electrophoresis.
- Excess wild-type p53 blocks initiation and maintenance of simian virus 40 transformation.
- Expression of tumor-specific transplantation antigen in cell lines transformed by wild-type of tsA mutant simian virus 40.
- UV-induced reversion of a temperature-sensitive late mutant of simian virus 40 to a wild-type phenotype.
- Studies of Nondefective Adenovirus 2-Simian Virus 40 Hybrid Viruses IV. Characterization of the Simian Virus 40 Ribonucleic Acid Species Induced by Wild-Type Simian Virus 40 and by the Nondefective Hybrid Virus, Ad2+ND1