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Biomedical subjects

J W Drake

Publications and source records attributed to J W Drake.

At least 73 records · Page 4Linked to original sources
PubMed1973

Ligase-defective bacteriophage T4. I. Effects on mutation rates.

Temperature-sensitive mutations in bacteriophage T4 gene 30 (polynucleotide ligase) were examined for their effects on spontaneous and proflavine-induced frameshift mutagenesis in the rII and ac (acridine resistance) cistrons. Only small (fourfold or less) effects on mutation rates were observed, even when selection artifacts involving suppression of gene 30 mutations by rII mutations were taken into account. The deoxyribonucleic acid ligase gene of T4 therefore appears to be only a minor determinant of frameshift mutation rates. This result is consistent with the particular nature of frameshift mutagenesis in bacteriophage T4.

Acridines↗
PubMed1972

Inactivation of bacteriophage T4 by ethyl methanesulfonate: influence of host and viral genotypes.

Inactivation of bacteriophage T4 by ethyl methanesulfonate (EMS) is a complex process which depends critically upon the conditions of treatment and upon both the viral and the host genotypes. EMS-inactivated particles are capable of multiplicity and cross-reactivation, indicating the need for caution in using EMS in certain types of mutation studies. The pyrimidine dimer excision systems of the phage and the host do not affect the EMS sensitivity of T4, but the T4x(+)y(+) system does. Mutational defects in the deoxyribonucleic acid (DNA) ligase and the DNA polymerase systems both of the virus and of its host also affect viral EMS sensitivity.

Alkylating Agents↗
PubMed1970

Mechanics of frameshift mutagenesis in bacteriophage T4: role of chromosome tips.

In contrast to observations in bacteria and fungi, frameshift mutations in bacteriophage T4 do not arise during genetic recombination. Nascent mutants, captured in the heterozygous condition, exhibit properties which indicate that the new lesions are located at the extreme tips of the chromosomes, and are segregated by a combination of recombination and replication.

Acridines↗
PubMed1970

Suppression of chemical mutagenesis in bacteriophage T4 by genetically modified DNA polymerases.

Two antimutagenic DNA polymerases of bacteriophage T4 markedly reduce transition mutagenesis by a variety of chemical mutagens. Spontaneous mutation and mutagenesis by 2-aminopurine, 5-bromodeoxyuridine, and thymine deprivation are strongly suppressed. Mutagenesis at G:C sites by ethyl methanesulfonate, and at A:T sites by nitrous acid, is moderately suppressed. Mutagenesis at G:C sites by hydroxylamine and by nitrous acid is not suppressed. These results support the notion that the indispensable DNA polymerase of bacteriophage T4 plays a crucial role in the selection of the correct base during DNA replication. The data also reveal that mutagenic specificities of chemical agents depend as much upon the characteristics of the enzymatic apparatus of DNA replication as they do upon the chemistry of primary mutational lesions.

Bromodeoxyuridine↗