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Biomedical subjects

A J Clark

Publications and source records attributed to A J Clark.

At least 343 records · Page 19Linked to original sources
PubMed1973

Detection and characterization of plasmids in Pseudomonas aeruginosa strain PAO.

Using a variety of techniques, it has been established that the sex factor FP2 has a density of 1.717 g/cm(3) (corresponding to a guanine plus cytosine [G + C] content of 58%) and a mean circular contour length of 28.5 +/- 0.6 mum (corresponding to a molecular weight of 59 x 10(6)). Another sex factor FP39 has a density of 1.719 g/cm(3) (corresponding to a G + C content of 60%) and a mean circular contour length of 26.5 +/- 0.5 mum (corresponding to a molecular weight of 55 x 10(6)). It appears that all, or nearly all, of the FP sex factor deoxyribonucleic acid occurs as covalent circular molecules under the conditions employed. In addition, these procedures have been used to demonstrate that strain PAO, a naturally occurring female (i.e., FP(-)) strain of Pseudomonas aeruginosa, harbors a number of cryptic plasmids having similar densities to the bulk of the cell deoxyribonucleic acid (1.726 g/cm(3)) and occurring as covalent circular molecules.

Adenine↗
PubMed1972

Indirect suppression of recB and recC mutations by exonuclease I deficiency.

recB(-)and recC(-) strains of Escherichia coli K12 are recombination deficient and sensitive to ultraviolet light and the drug, mitomycin C. We have reported that sbcB mutations indirectly suppress all three phenotypes and result in the loss of exonuclease I. In this publication we report the occurrence of other mutations that lead to loss of exonuclease I and indirectly suppress mitomycin and UV sensitivity but not recombination deficiency. These mutations (called xonA) are cotransducible with his and closely linked with sbcB. Both sbcB and xonA mutant strains appear to have identical residual amounts of nuclease activity on single-stranded DNA. It is hypothesized that exonuclease I possesses a second activity other than its known ability to degrade single-stranded DNA from a 3'-OH terminus. Accordingly, sbcB mutations would alter the second activity while xonA mutations would not.

Biodegradation, Environmental↗
PubMed1972

Conjugational complementation analysis of transfer-deficient mutants of Flac in Escherichia coli.

A series of 102 transfer-deficient (tra(-)) mutants of Flac (84 of which have been previously described) were classified as carrying frameshift, amber, ochre, UGA, and nonsuppressible mutations. Techniques were evolved for using cultures of F prime strains as efficient recipients in matings, for measuring the number of (F'/F') heterozygote cells in transient populations, and for measuring complementation between different Flac tra(-) mutants. These techniques were used to define nine tra cistrons and to assign most of the tra(-) mutations to one or other of these.

Bacteriological Techniques↗
PubMed1972

Genetic analysis of mutations indirectly suppressing recB and recC mutations.

Mutations in sbcB inactivate exonuclease I and suppress the UV-sensitive, mitomycin-sensitive, recombination-deficient phenotypes associated with recB and recC mutations. Mapping experiments have located sbcB about 0.4 minutes from the his operon at 38.0 on the standard map of E. coli. This places sbcB between supD and his. A four-point cross shows that sbcB lies between P2 attH and his. P2 eduction deleting the his operon beginning with P2 attH also deletes sbcB and produces the expected exonuclease I deficiency and suppression of recB(-). The occurrence of chemical-mutagen-induced and spontaneous mutations indirectly suppressing recB(-) and recC(-) is examined. Three lines of strains produce only sbcA mutations while only sbcB mutations occur in a fourth line. Explanations for this behavior are proposed in light of the ability of the first three lines to express sbcB mutations which they inherit by transduction.

Chromosome Mapping↗
PubMed1971

Genetic recombination in Escherichia coli: the role of exonuclease I.

The indirect suppression of recB(-) and recB(-)recC(-) mutations by the sbcB(-) allele is caused by the loss of a nuclease active on denatured DNA. Results from enzyme purifications and studies with a specific antiserum demonstrate that the activity present in sbcB(+) strains, and lost in sbcB(-) strains, is exonuclease I. It is likely that sbcB is the structural gene for exonuclease I. The loss of exonuclease I activity restores the recombination proficiency of Escherichia coli cells that has been lost by mutations in the recB and/or recC genes. This indicates that in the absence of the recB-recC-determined enzyme, exonuclease I prevents recombination. Hypothetical pathways illustrating this conclusion are presented.

Alleles↗
PubMed1971

Beginning a genetic analysis of conjugational transfer determined by the F factor in Escherichia coli by isolation and characterization of transfer-deficient mutants.

Eighty-four transfer-deficient mutants of Flac have been isolated; 27 of these bear amber mutations and 1 mutant is temperature-sensitive. All the mutants transfer between 10(-2) and <10(-5)% as well as wild-type Flac, all are curable by acridine orange treatment, and all are resistant to the female-specific phage phi(II). Some of the mutants are partially sensitive to female-specific phage tau. Sixty-three of the mutants are resistant to the male-specific phages f1, f2, and Qbeta; 15 are resistant only to f2; and 6 are sensitive to all three male-specific phages. Most of the mutants are still poor recipients in conjugation, but four of the mutants resistant to f1, f2, and Qbeta have become good recipients. Those mutants resistant to all three male-specific phages do not seem to make F-pili.

Acridines↗