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P L Bergquist

Publications and source records attributed to P L Bergquist.

At least 91 records · Page 5Linked to original sources
PubMed1979

Characterization of plasmids from antibiotic-resistant Shigella isolates by agarose gell electrophoresis.

Gel electrophoresis of DNA from 95 clinical isolates of Shigella sonnei and Shigella flexneri resistant to antibiotics revealed a heterogeneous plasmid population. Most of the plasmids were smaller than 6 megadaltons (Mdal). Six S. sonnei isolates with the most common antibiotic resistance pattern were characterized. They had two plasmids in common: one was a self-transmissible Fi+ plasmid of 46 Mdal encoding resistance to streptomycin and sulphafurazole. In addition, several cryptic plasmids ranging in size from 1.0 to 24.5 Mdal were present. Mobilization of the 5.5 Mdal SuSm plasmid and a 1.0 Mdal cryptic plasmid was demonstrated with all six S. sonnei isolates during conjugation. This mobilization was mediated by the 46 Mdal self-transmissible Fi+ R plasmid and also by a 24.5 Mdal Fi- plasmid carrying no known drug resistance determinants.

Anti-Bacterial Agents↗
PubMed1978

Degradation of missense mutant beta-galactosidase proteins in Escherichia coli K-12.

Ten out of 43 missense mutations in the lacZ gene of Escherchia coli gave rise to polypeptide chains that were degraded in vivo. While many of the mutants appeared to be fully or partially CRM-, there appeared to be no obvious correlation between degradation, map position, altered subunit association and the half-life of the mutant proteins.

Chromosome Mapping↗
PubMed1977

Role of dnaB43 in F'-plasmid incompatibility.

In order to perform complementation tests with mutations of DNA replication of F'-plasmids incompatibility must overcome. We report out in ability to duplicate the results presented by Palchoudhury and Iyer (1971) and Bezanson and Iyer (1975) who have claimed to demonstrate the autonomous replication two incompatible F'-plasmids in a strain carrying the temperature sensitive dna B43 allele. In addition, we describe experiments designed to measured complementation using transient heterozygotes and compatible plasmids. Assessment of our data and those of others in the light of a recent report by Uhlin and Nordström (1975) suggests that new approaches will have to be developed for the successful employment of complementation analysis in F-plasmid genetics.

Conjugation, Genetic↗
PubMed1977

Plasmid replication and Hfr formation in strains of Escherichia coli carrying seg mutations.

Several conditional-lethal mutantions that do not permit the replication of F-factors of Escherichia coli K-12 are located at a site called seg. This gene is located on the E. coli chromosome between ser B and thr. It is unrelated to other known genes involved in DNA replication. Strains carrying seg mutations were unable to replicate F'-lac+, several F'-gal+s, F'-his+ and bacteriophage gamma at 42 degrees. However, neither phage T4, ColE1, nor any of the R factors tested were prevented from replicating at 42 degrees C. When the kinetics of the loss of F-primes is studied in seg strains, it is found that the rate of curing depends on the size of the plasmid, larger F factors curing faster than smaller ones, and that Hfrs are formed at high frequencies. The Hfrs showed both F-genote enlargement and normal transfer of chromosomal markers. The F-genotes are unstable and segregate chromosomal markers at high frequencies. Some orthodox Hfrs were examined, and two that were known to revert to the F+ condition relatively frequently were found to generate enlarged F-genotes on mating, whereas two strains that were very stable with respect to the F+ state did not show F-genote formation. F-genote formation from seg Hfr stains is dependent on a functional recA gene, as F-genote formation was not seen with a seg-2, recA-1 Hfr. This is in contrast to F-genote enlargement shown by both orthodox Hfrs and an Hfr strain constructed by integration of a temperature-sensitive F'-gal+, whose F-genote enlargement is Rec-independent. Thus there may be more than one mechanism for the formation of enlarged F-genotes.

Chromosome Mapping↗
PubMed1977

Genetic inversion in the formation of an Hfr strain from a temperature-sensitive F' gal strain.

An Hfr strain (PB15) that carries a duplicated copy of the galactose operon genes flanking the integrated sex factor is unusually stable since it does not show excision of the repeated deoxyribonucleic acid segment. The right-hand galactose operon is in the normal orientation. Deletion mutations that eliminate the right-hand galactose genes, the sex factor, and some of the left-hand operon have been isolated. Mutants believed to have their left-hand galactose operon inverted were able to be induced for galactose epimerase synthesis by D-fucose but did not show escape synthesis on induction of bacteriophage lambda. Ribonucleic acid specific for the galactose operon was isolated after induction of lysogenic strains presumed to carry the galactose operon in the normal and inverted orientation. Hybridization to the isolated left and right strands of lambdapgal showed that the noninformational strand of the left-hand galactose operon of the deletion mutant of PB15 was transcribed on escape induction. These results show that inversion has occurred.

Chromosome Mapping↗
PubMed1976

Genetic and biochemical characterization of some missense mutations in the lacZ gene of Escherichia coli K-12.

Some preparations of beta-galactosidase from strains of Escherichia coli carrying point mutations in their lacZ genes did not precipitate with antibody as effectively as wild-type enzyme, but did not appear to be chain-terminating mutations as judged by polarity measurements and suppression. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis of crude extracts of induced Lac+ strains revealed that the monomer of beta-galactosidase ran as a band uncontaminated by other cellular proteins. This method was used to identify missense mutations in the alpha and beta portions of the lacZ gene. Six of 13 mutations investigated were judged to be missense by this criterion. Measurement of the degree of polarity, the ability to complement a nonsense mutation at the operator-distal extremity of the gene (omega-complementation), and suppressibility by 12 nonsense suppressors allowed the assignment of six other mutations as either number or ochre. The protein figments produced by these six nonsense mutations appeared to be degraded in vivo. One mutation that could not be classified was either a missense mutation whose protein product was degraded or a very leak nonsense mutation. Two lacZ alleles were suppressed by the ochre suppressors supM and supN, although they were missense by other criteria. The ability of supM to suppress both nonsense and missense mutations can be explained if it is derived from a tyrosine transfer ribonucleic acid with a modified base in the first position of the anticodon. The mutations assigned to the missense class were not suppressed by the missense suppressors supH, supQ, glyV, glyU, or glyT. Our results suggest that the criteria used in the past to distinguish between nonsense and missense mutations may not be conclusive even when used together.

Antigens, Bacterial↗
PubMed1972

Abnormal excision and transfer of chromosomal segments by a strain of Escherichia coli K-12.

PB15 is an Hfr strain of Escherichia coli K-12. It arose from an F' strain carrying a temperature-sensitive F-gal by an event which blocked the detachment of F-gal in the normally reversible integration process. In PB15, the detachment of F-gal by a second mechanism can now be detected: this mechanism results in the excision and transfer of extended chromosomal segments which include the integrated F-gal; the excised segments are inferred to have circularized. Their excision, which is independent of the recA(+) allele, occurs at an unusually high rate during conjugation; a mutant F-initiator protein is suggested as the cause of this phenomenon. After their establishment in recipients, the enlarged F-genotes undergo further deletions of included donor genes by a process which is again recA(+)-independent. In Rec(+), but not in Rec(-), cells, a high proportion of the deleted fragments are rescued by integration into the recipient's chromosome.

Acridines↗