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D W Mount

Publications and source records attributed to D W Mount.

At least 73 records · Page 4Linked to original sources
PubMed1978

Analysis of cell division in single clones of the Escherichia coli K-12 lexA mutant.

The growth of clones of lexA mutant and lexA+ cells was analyzed. During normal growth lexA mutant clones frequently divided early, producing smaller newborn cells than the lexA+ clones. Some newborn cells in the lexA clones did not elongate or divide at all, a response that was never observed in the lexA+ clones. When starved for thymidine, most of the lexA mutant clones elongated and subsequently divided. The majority of lexA+ clones also elongated but did not divide. The above results suggest that one of the functions of the lexA+ gene is coordination of DNA repair with cell division.

Cell Division↗
PubMed1978

Effect of tsl (thermosensitive suppressor of lex) mutation on postreplication repair in Escherichia coli K-12.

Cells of Escherichia coli K-12 carrying lexA or recA mutations are more sensitive to UV radiation than corresponding wild-type cells and are defective in postreplication repair. Supressor mutations (tsl) have been described previously which increase the UV resistance of lexA uvr+, lexA uvrA, and recAI uvr+ strains, but not the resistance of recA1 uvrA strains. We have studied the effect of the tsl-1 mutation on postreplication repair and find that the enhanced survival conferred by this mutation is correlated with an increased capacity for postreplication repair.

DNA Repair↗
PubMed1977

A mutant of Escherichia coli showing constitutive expression of the lysogenic induction and error-prone DNA repair pathways.

A mutant of E. coli (designated the STS mutant) has been isolated in which the phage induction and error-prone DNA repair pathways appear to be expressed constitutively without the cells having received an inducing signal. Phage lambda was not able to lysogenize this mutant, whereas a noninducible mutant of lambda, lambdacIind-, known to synthesize a repressor that is insensitive to the induction mechanism, lysogenized it normally. This result suggested that normal phage repressor was synthesized in the STS mutant but was then inactivated by the induction mechanism. The STS strain also had mutator characteristics, and showed spontaneous, error-prone repair of UV-damaged phage lambda. Derived from a lexA tif sfiA parent strain, the STS mutant carried an additional mutation spr at the lexA locus that resulted in a high level of expression of the induction pathways. The properties of this and related strains provide additional evidence that induction of phage and induction of error-prone DNA repair occur by a similar mechanism, and further suggest a model for the regulation of these pathways.

Coliphages↗
PubMed1977

Identification of the recA (tif) gene product of Escherichia coli.

Treatments that inhibit DNA synthesis in recA(+)lexA(+)Escherichia coli stimulate synthesis of a 40,000 molecular weight protein species (protein X). The protein X molecules produced by wild-type and mutant E. coli strains have been compared by two-dimensional gel electrophoresis. One recA mutant (DM1415 spr recA1) produced a protein X with a more acidic isoelectric point than protein X from the wild type, demonstrating that protein X is probably the product of the recA gene. Additional mutants carrying the recA-linked tif-1 mutation yielded a protein X that was more basic than the wild-type protein, indicating that the tif-1 mutation also alters the recA protein. Protein X molecules from the above mutants and wild-type E. coli have been shown to yield similar partial products upon limited proteolysis in sodium dodecyl sulfate, indicating they are the same protein species. These and additional studies suggest that (i) the tif-1 mutation alters a site on the recA protein that is sensitive to DNA synthesis inhibition, (ii) synthesis of recA protein is self-regulated, and (iii) synthesis of recA protein is also regulated by the lexA product with lexA-suppressor mutations such as spr resulting in constitutive synthesis of recA protein.

Bacterial Proteins↗
PubMed1977

Inactivation and proteolytic cleavage of phage lambda repressor in vitro in an ATP-dependent reaction.

We have reproduced in vitro the inactivation of bacteriophage lambda repressor that occurs in vivo when a lambda lysogen is treated with agents such as ultraviolet radiation that attack DNA. ATP and a divalent cation are required for the inactivation reaction. The ind- repressor is insensitive to the inactivation mechanism. A proteolytic cleavage of repressor accompanies inactivation in vitro, as it does in vivo.

Adenosine Triphosphate↗
PubMed1976

Inducible, error-free DNA Repair in tsl recA mutants of E. coli.

Host of cell reactivation and UV reactivation and mutagenesis of UV-irradiated phage mu were measured in tsl recAplus and tsl recA host mutants. Host cell reactivation was slightly more efficient in the tsl recA strain. Phage was UV-reactivated in the tsl recA strain with about one-half the efficiency of that in the wild type strain, but there was no corresponding mutagenesis of phage. UV-reactivation was also slightly lower and mutagenesis several-fold lower than normal in the tsl recAplus strain. To account for these observations, we propose that there is an inducible, error-free pathway of DNA repair in E. coli that competes with error-prone repair for repair of phage lesions.

Coliphages↗
PubMed1976

A method for the isolation of phage mutants altered in their response ot lysogenic induction.

Phage lambdacl+ gives clear plaques whereas phage lambdacIind- gives turbid plaques on a lawn of a mutant strain of E. coli K12. This strain, called STS, carries mutation spr in a tif sfi genetic background. I hypothesize that upon temperate phage infection, STS bacteria spontaneously inactivate phage repressor by the same mechanism involved in normal lysogenic induction which results in obligatory lytic growth of lambda+. The use of the STS mutant facilitates the isolation and genetic analysis of phage mutants with an abnormal response to lysogenic induction.

Coliphages↗
PubMed1975

Indirect suppression of radiation sensitivity of a recA- strain of Escherichia coli K12.

It has been shown previously that the radiation sensitivity of LexA strains of Escherichia coli K-12 can be suppressed by thermosensitive mutations (designated tsl) that are closely linked to the lexA locus. These are thought to be intragenic suppressors that reduce the activity of the diffusible product that gives rise to the LexA- phenotype (Mount et al., 1973). When a recA mutation is crossed into a suppressed tsl- strain, the extreme radiation sensitivity usually conferred by a recA mutation is considerably reduced without any detectable change in genetic recombination deficiency. Suppression of UV sensitivity depends upon the activity of the uvrA+ product. We propose that at least part of the radiation sensitivity of a recA- strain is due to a DNA repair defect that is different from inability to perform genetic exchanges and depends upon the presence of the lexA+ product. We hypothesize that the lexA+ product is a repressor of the synthesis of repair enzymes. In recA+ cells with DNA lesions, repressor is inactivated leading to enzyme induction but this does not occur in recA- cells. tsl mutations inactivate repressor leading to constitute enzyme synthesis and bypassing the need for recA+ product to inactivate the lexA+ product.

Cell Survival↗
PubMed1975

Ultraviolet light-induced mutation in UV-resistant, thermosensitive derivatives of lexA-strains of Escherichia coli K-12.

It was shown previously that a major class of UV-resistant derivatives of lexA- strains of E. coli K-12 is defective in cell division at 42.5 degrees. The thermosensitive mutations, judging by genetic mapping and complementation tests, are believed to be intragenic suppressor mutations that lower the activity of the diffusible product that results in the LexA- phenotype (Mount et al., 1973). Several thermosensitive derivatives have been characterized in regard to their susceptibility to mutation induction by UV at the permissive growth temperature (30 degrees). Although the strains tested are approximately as resistant to UV as lexA+ strains, they showed a level of mutation induction that was considerably lower. By means of genetic complementation tests it was demonstrated that the low levels of UV mutagenesis in lexA- strains and their thermosensitive derivatives result from the synthesis of a diffusible product. One possible interpretation of these results is that a diffusible product in lexA- strains prevents the induction of error-prone repair. Altering the activity of this product by tsl mutations can lead to increased, but not normal, levels of error-prone repair.

Bacterial Proteins↗
PubMed1975

Effect of tsl mutations in decreasing radiation sensitivity of a recA- strain of Escherichia coli K-12.

It has been shown previously that the radiation sensitivity of lexA- strains of Escherichia coli K-12 can be suppressed by thermosensitive mutations (designated tsl) that are closely linked to the lexA locus and are thought to be intragenic suppressors of lexA mutations (Mount et al., 1973). When a recA mutation is crossed into a suppressed tsl- strain, the extreme radiation sensitivity usually conferred by a recA mutation is decreased, but there is no detectable change in genetic recombination deficiency. Increased resistance to UV in the tsl-reA-strains depends upon ability to synthesize active uvrA+ product.

Cell Division↗
PubMed1975

Production of cells without deoxyribonucleic acid during thymidine starvation of lexA- cultures of Escherichia coli K-12.

When thymidine-requiring lexA- strains were starved for thymidine, the kinetics of survival were similar to those of a nearly isogenic lexA+ strain. The size distribution of cells in the lexA- and lexA+ cultures were, however, quite different. Whereas most of the cells in the starved lexA+ cultures grew into long filamentous forms (longer than 4.0 mum), many of the lexA- cells were found to have a normal rod shape (4.0 mum or shorter). It was shown that lexA- cells undergo more divisions during thymidine starvation than lexA+ cells. Furthermore, using an autoradiographic method to analyze deoxyribonucleic acid (DNA) distribution in the starved cells, we demonstrated that cells without DNA are produced in both normal and starved lexA- cultures at a much higher frequency than in lexA+ cultures. Some of these cells may be produced by breakdown of DNA, but we favor the hypothesis that they result from an abnormal cell division process. Since lexA mutations are dominant, we conclude that a diffusible product decreases the synthesis or activity of an inhibitor of cell division in lexA- strains when DNA synthesis is blocked by thymidine starvation.

Cell Count↗
PubMed1972

Dominant mutations (lex) in Escherichia coli K-12 which affect radiation sensitivity and frequency of ultraviolet lght-induced mutations.

Three mutations, denoted lex-1, -2 and -3, which increase the sensitivity of Escherichia coli K-12 to ultraviolet light (UV) and ionizing radiation, have been found by three-factor transduction crosses to be closely linked to uvrA on the E. coli K-12 linkage map. Strains bearing these mutations do not appear to be defective in genetic recombination although in some conjugational crosses they may fail to produce a normal yield of genetic recombinants depending upon the time of mating and the marker selected. The mutagenic activity of UV is decreased in the mutant strains. After irradiation with UV, cultures of the strains degrade their deoxyribonucleic acid at a high rate, similar to recA(-) mutant strains. Stable lex(+)/lec(-) heterozygotes are found to have the mutant radiation-sensitive phenotype of haploid lex(-) strains.

Alkanesulfonates↗
PubMed1969

Genetic analysis of recombination-deficient mutants of Escherichia coli K-12 carrying rec mutations cotransducible with thyA.

The rec mutations carried by 20 strains of Escherichia coli K-12 which are defective in genetic recombination and sensitive to ultraviolet light and X rays, and whose lambda lysogens show spontaneous phage production, have been mapped near thyA. In 15 of the strains, the rec mutation fails to complement recB21 but complements rec-22. The other five strains carry a rec mutation which complements recB21 but not rec-22. These mutations map closer to thyA than those which fail to complement recB21. They therefore appear to be defective in a different recombination gene, denoted recC. The order of recB and recC on the linkage map of E. coli K-12 is thyA-recC-recB-argA.

Alleles↗