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P A Swenson

Publications and source records attributed to P A Swenson.

At least 19 recordsLinked to original sources
PubMed1986

Lack of UV-induced respiration shutoff in a recF strain of Escherichia coli: temperature conditional suppression at 30 degrees C by the sfrA mutation.

A mutation in the recF gene of Escherichia coli results in a radiation-sensitive strain. The RecF pathway and the RecBC pathway account for nearly all of the conjugative recombination occurring in E. coli. recBC cells are radiation-sensitive and carry only out a small amount of recombination but these deficiencies are suppressed by an sbcB as recombination is shunted to the RecF pathway. A recBC sbcB recF strain is very radiation-sensitive and is devoid of recombination ability. These deficiencies are suppressed by the srfA mutation; srfA is a recA allele. UV-induced respiration shutoff is a recA+, lexA+ and recBC+ dependent. We report in this paper that respiration does not shutoff in a recF strain at 37 and 30 degrees C. an srfA mutation suppresses this lack of respiration shutoff effect in a recF srfA mutant at 30 degrees C but not at 37 degrees C; no suppression by this mutation occurs at either temperature in a recF recBC sbcB strain. An srfA strain also does not shut off its respiration at 37 degrees C and shows a temperature conditional UV-induced respiration shutoff response at 30 degrees C. The srfA mutation is thought to cause an altered RecA protein to be produced and we suggest that at 37 degrees This altered protein is temperature sensitive. We conclude from the results in this paper that the recF gene product is required for UV-induced respiration shutoff and that the RecA protein plays a special role in the induction process.

Bacterial Proteins↗
PubMed1984

Respiration shutoff in Escherichia coli K12 strains is induced by far ultraviolet radiations and by mitomycin C.

Ultraviolet radiations (254 nm) (UV) cause respiration to shutoff in Escherichia coli B/r. It has been reported [P.A. Swenson, Photochem. Photobiol., 33 (1981) 855-859 and J. Barbé, A. Vericat and R. Guerrero, Mutation Res., 120 (1983) 1-5] that E. coli K12 strains do not shut off respiration after UV. The latter authors also reported that mitomycin C did not cause this 'SOS' response. In this paper we report that higher UV fluences than were previously used will cause respiration shutoff in K12 strain W3110 and that cyclic AMP increases the sensitivity of respiration shutoff of irradiated cell suspensions. We also report that mitomycin C shuts off respiration in this strain. Neither UV nor mitomycin C causes respiration shutoff in the recA56 derivative of W3110. Thus respiration shutoff is a recA dependent response to UV and mitomycin C in E. coli K12 strains.

Escherichia coli↗
PubMed1981

The muc+ gene of plasmid pKM101 prevents respiration shutoff in far ultraviolet-irradiated Salmonella typhimurium.

The plasmid PKM101 is known to protect Escherichia coli and Salmonella typhimurium against killing by far UV irradiation and to enhance UV-induced mutagenesis. The muc+ gene of the plasmid is responsible for both of these effects. This paper shows that respiration of S. typhimurium shuts off about an hour after UV irradiation and that pKM101 prevents the shutoff. Plasmids which contained Tn5 translocatable elements, either in (and having produced a muc mutation) or flanking the muc+ gene, have been introduced into S. typhimurium. The muc mutant plasmid, which does not protect its host against UV killing and does not enhance UV induced mutagenesis, also does not protect against UV induced respiration shutoff. Likewise, plasmids in which the Tn5 translocatable elements flank the muc+ gene protect against shutoff of respiration. Thus the muc+ gene of pKM101 is responsible for protection against UV induced shutoff of respiration in S. typhimurium.

DNA Repair↗
PubMed1979

Antipain lethality to Escherichia coli: dependence upon cyclic adenosine 3',5'-monophosphate and its receptor protein.

Antipain kills Escherichia coli K-12 cells in an exponential manner beginning 1 h after its addition. Mutant strains, delta cya and crp, which are unable to synthesize cyclic adenosine 3',5'-monophosphate (cAMP) and the cAMP receptor protein, respectively, are not affected. Addition of cAMP (5 mM) to antipain-treated mutant strains causes killing of delta cya cells, but not crp cells. Thus the lethal effect of antipain is dependent upon cAMP and its receptor protein.

Cyclic AMP↗
PubMed1977

Continuous-flow system for large-scale ultraviolet irradiation of bacterial cells.

A quartz-flow-cell system for irradiation of large volumes of Escherichia coli cultures with ultraviolet light is described. With this system kilogram quantities of irradiated cells can be obtained for biochemical studies. Changes in respiration and in specific activities of superoxide dismutase and catalase, after an ultraviolet treatment that reduced viability of culture samples to 0.2%, were in good agreement with those for cultures irradiated (52J/m2) by a conventional small-scale method to produce the same reduction in viability.

Bacteriological Techniques↗
PubMed1977

Delayed ultraviolet light-induced cessation of respiration by inadequate aeration of Escherichia coli.

Inadequately aerated Escherichia coli B/r cultures did not shut their respiration off 60 min after ultraviolet light (52 M/m2 at 254 nm) as they did when well supplied with oxygen. Since cessation of respiaration is associated with cell death, the result suggested that oxygen toxicity by superoxide radicals generated by cell metabolism might be responsible for cell death. The specific activity of superoxide dismutase, which scavenges O2- radicals, increased twofold after 90 min of adequate aeration, but the specific activity of catalase remained constant. Respiration and viability of irradiated cells were affected not at all by the presence of superoxide dismutase and only slightly by the presence of catalase. Metal ions such as Mn2+ and Fe2+ inducers of superoxide dismutase, had no effect on respiration and viability. When irradiated cells were incubated under N2 for 90 min, the respiration, growth, and viability time-course responses were the same as for the cells not exposed to anareobiosis. We conclude that superoxide anions generated at the time of irradiation play no part in cessation delays the ultraviolet light-induced synthesis of proteins responsible for the irreversible cessation of respiration.

Anaerobiosis↗
PubMed1977

Role of cyclic adenosine 3',5'-monophosphate on cessation of respiration in ultraviolet-irradiated Escherichia coli.

The addition of cyclic adenosine 3',5'-monophosphate (cAMP) to ultraviolet-irradiated Escherichia coli B/r cultures causes additional cells to cease respiring and to die. These effects of cAMP are greater on glucose-grown cells, where the effects of ultraviolet radiations alone are smaller and where the intracellular concentrations of cAMP are known to be lower.

Cyclic AMP↗
PubMed1976

Centrifugal separation of irradiated cultures of Escherichia coli cells into viable and nonviable populations.

Incubation of ultraviolet-irradiated Escherichia coli B/r cultures with 0.7% Triton X-100 resulted in a large decrease in turbidity. Under phase-contrast optics, most of the irradiated detergent-treated cells were smaller than normal and of low phase density; only a small percentage were normal or larger than normal and of normal phase density. Irradiated cells not treated with detergent showed fewer pronounced morphological changes. Irradiated cells treated with detergent lost large amounts of proteins and ribonucleic acid, but not of deoxyribonucleic acid. Such cultures could be separated by centrifugation into populations of (i) slowly sedimenting cells consisting of small, phase-light cells of low viability and (ii) large cells of normal phase density and high viability (100%). A similar separation was effected in gamma-irradiated cultures.

Bacterial Proteins↗
PubMed1976

Pyrimidine dimer excision in surviving and nonsurviving cells of ultraviolet-irradiated cultures of Escherichia coli.

We compared dimer excision in viable and nonviable cells fractions separated from Escherichia coli B/r cultures exposed to ultraviolet (UV) irradiation. For cells grown on minimal medium with glycerol as a carbon source, both fractions from the irradiated (20 J/m2, 5% survival) culture excised 60 to 70% of the thymine dimers from prelabeled DNA within 120 min. This percentage was, within experimental error, the same as that obtained from unseparated cultures. When isolated viable and nonviable populations were given a second UV exposure (20 J/m2) both types of cells were again able to excise dimers. The UV survival curve for the isolated viable population indicates that these cells are no more sensitive to radiation than exponentially growing cells not previously exposed to UV. The extent of dimer excision after UV irradiation was also the same in viable and nonviable cells separated from cultures grown on a glucose minimal medium in which both populations excised about 85% of the dimers within 120 min. These results show that the extent of removal of pyrimidine dimer from deoxyribonucleic acid is not precisely correlated with survival of repair-competent bacterial cells after exposure to UV light.

DNA Repair↗