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. 1984 Oct 11;12(19):7503–7515. doi: 10.1093/nar/12.19.7503

Inhibition of polyoma DNA synthesis by base pair substitutions at the replication origin.

H Luthman, M Osterlund, G Magnusson
PMCID: PMC320177  PMID: 6093042

Abstract

The effect of base pair substitutions on the function of the polyoma virus origin of DNA replication was studied. The mutations were all C-G to T-A transitions, induced by bisulfite treatment of recombinant DNA molecules. The mutagenesis was directed to short single-stranded gaps in duplex DNA, or to loops in heteroduplex molecules. Modification of a 34 base pair sequence of dyad symmetry led to cis-acting inhibition of viral DNA synthesis, ranging from slight defects to total inactivation. One of the mutants was temperature sensitive. Mutants with base changes in an adjacent DNA segment, including an 18 base pair long purine-pyrimidine tract, had similar, but less severe, deficiences. In contrast to the effect of mutations in the homologous region of the simian virus 40 genome, there was no strict relationship between mutation of the putative large T-antigen-binding base sequence GPuGGC and defective viral DNA synthesis.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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