Frameshift mutagenesis of lambda prophage by 9-aminoacridine, proflavin and ICR-191

1984 ◽  
Vol 195 (3) ◽  
pp. 418-423 ◽  
Author(s):  
Thomas R. Skopek ◽  
Franklin Hutchinson
1981 ◽  
Vol 90 (1) ◽  
pp. 1-10 ◽  
Author(s):  
Peter R. Young ◽  
Rong-Ine Ma ◽  
Peter Marfey ◽  
Neville R. Kallenbach

1988 ◽  
Vol 9 (7) ◽  
pp. 1153-1158 ◽  
Author(s):  
Caroline A. Stanton ◽  
Colin R. Garner ◽  
Carl N. Martin

Genetics ◽  
1983 ◽  
Vol 103 (3) ◽  
pp. 353-366
Author(s):  
Lynn S Ripley ◽  
Nadja B Shoemaker

ABSTRACT T4 DNA polymerase strongly influences the frequency and specificity of frameshift mutagenesis. Fifteen of 19 temperature-sensitive alleles of the DNA polymerase gene substantially influenced the reversion frequencies of frameshift mutations measured in the T4 rII genes. Most polymerase mutants increased frameshift frequencies, but a few alleles (previously noted as antimutators for base substitution mutations) decreased the frequencies of certain frameshifts while increasing the frequencies of others. The various patterns of enhanced or decreased frameshift mutation frequencies suggest that T4 DNA polymerase is likely to play a variety of roles in the metabolic events leading to frameshift mutation. A detailed genetic study of the specificity of the mutator properties of three DNA polymerase alleles (tsL56, tsL98 and tsL88) demonstrated that each produces a distinctive frameshift spectrum. Differences in frameshift frequencies at similar DNA sequences within the rII genes, the influence of mutant polymerase alleles on these frequencies, and the presence or absence of the dinucleotide sequence associated with initiation of Okazaki pieces at the frameshift site has led us to suggest that the discontinuities associated with discontinuous DNA replication may contribute to spontaneous frameshift mutation frequencies in T4.


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