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Biomedical subjects

J R Christensen

Publications and source records attributed to J R Christensen.

At least 37 records · Page 2Linked to original sources
PubMed1986

T1 pip: a mutant which affects packaging initiation and processive packaging of T1 DNA.

The pip mutation of phage T1 is located between the tar (gene 2.5) and am6 (gene 3) mutations in the region of the T1 genome which codes for early functions. The tar and pip mutations are additive in increasing the efficiency of transduction by T1. When T1 carries the pip mutation the initiation of DNA packaging by the phage at the non-T1, esp-lambda site is more efficient than when the phage is pip+; the small average burst size of 8 to 10 by T1pip suggests that pip causes a reduction in the efficiency with which T1 utilizes pac, the normal packaging initiation site of the phage. The presence of the BglII-D fragment (cut at one end at pac and the other by BglII) after digestion of T1pip DNA by BglII shows that T1pip continues to initiate DNA packaging at pac. The increased molarity of BglII-D coupled with the absence of the BglII-C fragment (which contains DNA on both sides of pac and can only be cut from processively packaged genomes) shows that T1pip packages only genomes which are initiated at pac and is defective in processive packaging.

Bacterial Proteins↗
PubMed1986

Specific inhibition of tyrosine kinase activity by an antibody to the v-ros oncogene product.

Antibodies present in two peritoneal exudates of rats bearing abdominal tumors induced by UR2-transformed rat cells were characterized. The ability to immunoprecipitate p68gag-ros and to inhibit the protein and phospholipid kinase activities of this protein was investigated. One of the exudates specifically inhibited tyrosyl phosphorylation by p68gag-ros but not the activity of other known tyrosyl kinases, such as p150gag-fps of UR1 avian sarcoma virus, p60src, and the insulin receptor. It precipitated p68gag-ros but not Pr76 or other gag-related proteins from UR2-infected cells. Phosphorylation of phosphatidylinositol was not affected by this exudate, suggesting that this activity is not intrinsic to p68gag-ros. Another exudate precipitated p68gag-ros but not gag-related proteins from UR2-infected cells or p140gag-fps from Fujinami sarcoma virus-infected cells. These results demonstrated that the antibodies in these exudates recognized epitopes present in the ros portion of the fused protein p68gag-ros, but only one of the two exudates inhibited the intrinsic tyrosyl kinase of p68gag-ros.

Animals↗
PubMed1985

Characterization of insulin uptake into subcellular fractions of perfused rat liver using two different iodinated tracers.

The binding and uptake of insulin in perfused rat liver has been investigated with specifically labelled 125I-A14-tyrosyl insulin as a tracer and compared with a commercially available iodo-insulin preparation. The commercial preparation did not show saturation uptake kinetics and the clearance from the perfusate remained low and constant throughout a wide concentration range. A14 labelled insulin showed saturation kinetics and high clearance at low carrier concentration, falling rapidly with increasing carrier concentration and reaching a steady state value of 1 ml/min. These results emphasize the importance of using specifically labelled insulin in physiological and biochemical studies of hepatic insulin metabolism. Perfusion with A14 tyrosine-labelled insulin at 4 degrees C showed apparent saturation with binding to the plasma membrane fraction. Perfusion at 37 degrees C also showed apparent saturation with uptake predominantly to the ligandosome fraction. These results implicate the plasma membrane-ligandosome pathway in the hepatic uptake of insulin at both physiological and pharmacological concentrations of the hormone.

Animals↗
PubMed1985

Untargeted mutagenesis induced by UV in the lacI gene of Escherichia coli.

Using a nonselective method, we have estimated the proportion of untargeted mutations in the lacI gene of E. coli by transferring either irradiated or unirradiated F' pro lac plasmids from an excision deficient donor to an excision deficient pro lac deleted recipient that had been irradiated and allowed to induce recA dependent functions for 30 min. We find that about 10 percent of the mutations induced by either 3.5 Jm-2 or 7 Jm-2 UV are untargeted.

Bacterial Proteins↗
PubMed1985

Conjugation-dependent enhancement of induced and spontaneous mutation in the lacI gene of E. coli.

The frequency of lac mutations induced in an F'lacIS plasmid, transferred by conjugation from UV-irradiated, excision-deficient donors to excision-deficient, delta pro lac recipients, is 2-3 fold higher than that typical of nonmating cells which contain the plasmid. These additional induced mutations can probably be ascribed to errors made during the first, or repliconation, synthesis that takes place in the recipient during the course of plasmid transfer. We also find that spontaneous mutation rates are enhanced in conjugating cells, indicating that fewer errors are corrected, or more made, during transfer replication.

Bacterial Proteins↗
PubMed1985

Identity of the photoproduct that causes lacI mutations in UV-irradiated Escherichia coli.

Estimates of the capacity of photoreactivation to act specifically on premutational lesions were obtained by conjugational transfer of an F' lac plasmid from a UV-irradiated, photoreactivated donor to a delta (pro-lac) recipient that had been UV irradiated and allowed to induce SOS functions for 30 min. This treatment reduced the frequency of induced lacI mutations by 70 to 80%, indicating that cyclobutane dimers cause most mutations in this system.

Escherichia coli↗
PubMed1981

Requirement for protein synthesis for survival of unmodified bacteriophage T1 in a restricting host.

At high multiplication of infection, a substantial fraction of restricting cells (P1 lysogens) could be productively infected by unmodified coliphage T1 (T1.0) provided that protein synthesis was uninhibited during the first 5 min of infection. Successful infection under restricting conditions was accompanied by more genetic recombination than was seen under nonrestricting host, the recombination frequency declined for markers on T1.0 genomes; no effect was seen on recombination between markers on modified (T1.P) genomes. This suggested that recombination between unmodified genomes may be essential for their survival under conditions of host restriction. In a restricting host, genetic markers on T1.0 could recombine with T1.P even when the rescuing phage was added 6 min after T1.0 infection. However, even marker rescue recombination was diminished when protein synthesis was inhibited during early infection. Since DNA restriction is an early event, protein synthesis may be required soon after infection of a restricting host by T1.0 in order to preserve restriction-damaged DNA in a form that can participate in recombination. Experiments are also described that rule out some possibilities for the role of such a protein(s).

Chloramphenicol↗
PubMed1980

Studies on recombination in heterologous crosses of Rous sarcoma virus.

Ts mutants in src from the Prague and Schmidt-Ruppin strains of Rous sarcoma virus (RSV) were used to superinfect chicken and quail cells chronically infected with the Bryan strain of RSV. No wild-type recombinants and few double-defective virions were produced. These results indicate that genetic recombination does not occur with high frequency in these heterologous crosses even if all infectious virus is derived from doubly infected cells.

Animals↗
PubMed1980

Exclusion of bacteriophage T1 by bacteriophage lambda. II. Synthesis of T1-specific macromolecules under N-mediated excluding conditions.

The results of experiments investigating T1 macromolecular synthesis under N-mediated excluding conditions failed to demonstrate a substantial alteration in the T1 mRNA production in excluding cultures at any stage in the T1 infectious cycle. The number of T1 DNA sequences in the excluding culture was found to be one-third to one-half that found in T1-infected cultures. The most severe reduction in T1-specific macromolecules was seen in protein synthesis. Total incorporation of labeled amino acids was reduced sixfold, and gel experiments confirmed that the T1-specific proteins capable of detection are reduced in excluding cells.

Bacteriophage lambda↗
PubMed1979

Transduction of bacteriophage lambda by bacteriophage T1.

When bacteriophage T1 was grown on bacteriophage lambda-lysogenic cells, phenotypically mixed particles were formed which had the serum sensitivity, host range, and density of T1 but which gave rise to lambda phage. T1 packaged lambda genomes more efficiently both when the length of the prophage was less than that of wild-type lambda and when the host cell was polylysogenic. Expression of the red genes of lambda or the recE system of Escherichia coli during T1 growth enhanced pickup of lambda by T1, whereas packaging was reduced in recB cells. If donors were singly lysogenic, the expression of transduced lambda genomes as a PFU required lambda-specified excisive recombination, whereas lambda genomes transduced from polylysogens required only lambda- or E. coli-specified general recombination to give a productive infection.

Coliphages↗
PubMed1979

Recombination in bacteriophage T1 in the presence of host restriction.

When unmodified phage T1 infects restricting host cells at high multiplicities of infection, there is an increase in recombination frequency in all regions of the T1 map compared to the level of recombination in standard crosses when short distances are examined. The enhancement of recombination frequency is not uniform for all regions but is greatest for markers near the center of the map and not so great for markers near the ends. Crosses between markers at the extremities of the map show that there is no increase in recombination frequency under restriction conditions. An examination of phage T1 heterozygotes suggests that an increase of ends created by the process of P1 restriction increases recombination. When T1 crosses are done in the absence of host restriction, recombination defects in the host have no effect on phage recombination and we conclude that phage T1 codes for its own recombination genes. Host recombination functions are also dispensable for the recombination occurring during infection of restricting host cells by unmodified phage at high multiplicities of infection.

Crosses, Genetic↗