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J R Christensen

Publications and source records attributed to J R Christensen.

54 records · Page 3Linked to original sources
PubMed1978

Exclusion of bacteriophage T1 by bacteriophage lambda. I. Early exclusion requires lambda N gene product and host factors involved in N gene expression.

Two modes of exclusion of T1 by lambda are distinguished. "Early" exclusion depends on gene N, but not on gene Q. It is at least partially ineffective against T1am23. "Late" exclusion depends on gene Q and effects T1am23 as well as T1+. Early exclusion is a direct effect of N gene product, rather than N gene being required for the expression of some other lambda gene. Three host mutations, groN, nusA, and nusB, known to interfere with lambda replication by affecting N gene expression, also interfere with the ability of lambda to exclude T1.

Coliphages↗
PubMed1976

Red system of bacteriophage lambda complements the growth of a bacteriophage T1 gene 4 mutant.

The ability of phage lambda to complement the growth of T1am23, a T1 gene 4 mutant with a DNA arrest phenotype, has been shown to require both lambda Red functions, redX and redB. lambdagam function, however, is not required. Therefore, the lambda Red function can substitute for T1 gene 4 function. However, T1+ does not substitute for lambda Red in allowing lambda to grow in a polA host.

Chromosome Mapping↗
PubMed1974

Physiological study of cooperative infection by restricted bacteriophage T1.

The ability of certain phages to successfully infect a restricting host at a high multiplicity of infection is known as cooperative infection or cooperation. We have examined the ability of unmodified T1 (T1.0) to participate in cooperative infection in cells possessing the P1 restriction system. We have found that cooperation is dependent upon protein synthesis during the first few minutes after phage infection. However, we have been unable to attribute the necessary protein to a known T1 cistron. Degradation of the restricted T1 genome is approximately equally extensive whether cooperative infection occurs or whether it is blocked by chloramphenicol. It is postulated that an inducible host repair mechanism may be responsible for the phenomenon of cooperative infection.

Chloramphenicol↗
PubMed1974

Complementation by restricted phage T1.

The ability of restricted phage T1hr to complement stocks of T1am mutants carrying the P1 modification has been tested in mixed infection of Escherichia coli B(P1). Of the 18 genes tested, 15 could be complemented to give successful infection of approximately 10 to 25% of the cells, and 2 other genes consistently gave at least 5% complementation. The progeny phage produced in these infections was predominantly of the hr(+)am genotype. A mutant in gene 12 could be complemented very poorly, if at all. With one double mutant stock, the complementation obtained was nearly as good as the more poorly complemented of the two corresponding single mutants.

Coliphages↗
PubMed1974

Interactions between the vegetative states of phages lambda and T1.

Bacteria containing phage lambda in the vegetative state were produced either by induction of lambda lysogens or by infection of sensitive cells with lambda. These cells were superinfected with T1, and assayed for the production of lambda, T1, or both. Although most of the cells produced only lambda or T1, approximately 10% of the infectious centers were dual yielders. Examination of the progeny phage produced by the population of mixedly-infected cells showed that there was little, if any, phenotypic mixing, as determined by adsorption phenotype. T1am mutants in a variety of T1 genes were tested for their ability to exclude lambda, but none were defective in this ability. One gene of T1, gene 4, can be complemented by lambda.

Bacteriolysis↗
PubMed1970

Synthesis of messenger ribonucleic acid after bacteriophage T1 infection.

Synthesis of host-specific and phage-specific messenger ribonucleic acid (mRNA) was studied in bacteria infected by unmodified (T1 . B) or modified [T1 . B(P1)] bacteriophage T1. In a "standard" infection of Escherichia coli B by T1 . B (no host-controlled modification involved), the rate and amount of T1 mRNA synthesis was intermediate between those values reported for infections by a virulent phage such as T4 or a temperate phage such as lambda. The initial rate of mRNA synthesis was slightly increased after T1 . B(P1) infection of E. coli B in comparison with T1 . B infection of the same host. Little or no phage mRNA synthesis could be detected in T1 . B infection of E. coli B(P1). Phage mRNA synthesis in T1 . B(P1)-infected E. coli B(P1) cells was approximately the same in amount as that seen in T1 . B(P1) infection of E. coli B. Synthesis of host-specific mRNA continued throughout the latent period in all infections studied. However, the enzyme beta-galactosidase could not be induced, except after T1 . B infection of E. coli B(P1). In an attempt to understand the apparent differences in mRNA synthesis after infection of E. coli B by phages T1 . B or T1 . B(P1), the effect of altered T1 deoxyribonucleic acid (DNA) methylation on mRNA synthesis was studied. Methyl-deficient T1 DNA, made in cells infected with ultraviolet-irradiated phage T3, inhibited (14)C-uridine incorporation more strongly than normal T1. One passage of methyl-deficient T1 through E. coli B restored uracil incorporation rates to those seen with ordinary T1. This suggests that methylation of T1 DNA can influence the rate of phage mRNA synthesis. However, attempts to relate the difference in mRNA synthesis seen between T1 . B and T1 . B(P1) in E. coli B to the activity of the P1 modification gene were not conclusive.

Carbon Isotopes↗
PubMed1969

Infection by bacteriophage P1 and development of host-controlled restriction and modification and of lysogenic immunity.

Shigella dysenteriae cells were infected with phage P1 or P1cl. The outcome of superinfection of these cells with phage T1.Sh or T1.Sh(P1) or P1cl was studied as a function of time after the initial infection. Cells undergoing either a lytic response or a lysogenic response to the primary infection develop the ability to specifically restrict T1.Sh between 30 and 45 min. Between 15 and 30 min, the cells seem to develop the ability to produce T1.Sh(P1) after infection by T1.Sh. However, reasons are given for believing that this apparent time difference is consistent with a simultaneous development of the two capacities (restriction and modification) within the cell. This development occurs between 30 and 45 min. Cells infected with P1cl and superinfected 45 or more min later with T1.Sh(P1) can yield both P1cl and T1. Cells infected with P1 become resistant to infection by P1cl within 5 to 10 min. It is argued that this early immunity is not necessarily different in mechanism from true lysogenic immunity.

Bacteriophages↗
PubMed1968

Multiplication of bacteriophage P1 mutants in Shigella dysenteriae strain Sh(P1).

From bacteriophage P1, 10 mutants (P1cl) were isolated which are impaired in their ability to lysogenize Shigella dysenteriae Sh and which fail to make plaques when plated on Sh(P1). When Sh(P1) is infected with P1cl, a considerable proportion of the infected cells is converted into infectious centers, which eventually release P1cl but not P1. This phage release occurs over a period of several hours, during which a manyfold multiplication of infectious centers takes place. In the course of this multiplication, surviving bacteria, lysogenic for P1 only, are produced by segregation. At high multiplicity of infection, Sh(P1) are killed without producing any phage.

Bacteriophages↗
PubMedDate not supplied

Enamel pretreatment with sodium hypochlorite to enhance bonding in hypocalcified amelogenesis imperfecta: case report and SEM analysis.

Bonding composite resin to enamel of teeth affected by amelogenesis imperfecta (AI) is often problematic, especially in cases with poorly mineralized, friable enamel. Difficulty in bonding hypomineralized enamel can significantly limit the restorative and orthodontic treatment options for AI patients. In this report, we document a novel approach to bonding AI enamel by pretreating the tooth surface with 5% sodium hypochlorite (NaOCl), resulting in improved bonding of an orthodontic bracket to a previously impacted maxillary canine.

Acid Etching, Dental↗