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A Ronen

Publications and source records attributed to A Ronen.

31 records · Page 2Linked to original sources
PubMed1978

Site specificity and variability in the mutator and antimutator effects of phage T4 gene 43 mutants.

Spontaneous, 2-aminopurine- and 5-bromouracil-induced mutations at six rII nonsense codons were studied in phage T4 strains possessing wild-type and mutant gene 43 alleles. The mutation pathways studied included interconversions and reversions of nonsense codons. The tsCB87 allele, which specifies an antimutator DNA polymerase, reduced base-analogue-induced mutation frequencies along all pathways. However, GC base pairs were less affected than AT base pairs. The frequency of spontaneous UAA leads to UAG conversions was also reduced by tsCB87, but that of spontaneous UAA leads to UAG UGA conversions was often increased. Mutation in the presence of the mutator allele tsL56 was increased along all pathways, with no preference for either AT or GC base pairs. Mutation frequencies in the presence of the two mutant DNA polymerases were highly variable. A strong correlation was found between 2-aminopurine-induced mutation frequencies in ts+ tsCB87 phage along the reversion and UAA changed to UAG (but not UAA changed to UGA) pathways.

2-Aminopurine↗
PubMed1976

Mutagen specificity and position effects on mutation in T4rII nonsense sites.

In 14 sites in the T4rII region, spontaneous and induced interconversions of ochre (UAA) and opal (UGA) alleles, as well as the reversion of the nonsense sites to r+, were studied. The mutagens employed were 2-aminopurine (2AP), 5-bromouracil (5BU), N-methyl-N'-nitro-N-nitrosoguanidine (NTG) and hydroxylamine (HA). With the test system employed, mutagen specificity (i.e., the preferential induction of A: T leads to G: C or G: C leads to A: T mutation at a given site) can be studied. Simultaneously, the response of similar base pairs at various locations in the same or in different nucleotide triplets throughout the rII region, to a given mutagen, can be compared. 2-Aminopurine can induce transitions of both A: T and G: C base pairs at high rates. This mutagen shows no preference for either direction. Furthermore, there is a correlation between the response to 2AP of an A: T pair occupying a given site, and that of a G: C pair occupying the same site. NTG and HA induce G: C leads to A: T transitions almost exclusively. However, there is a correlation between the low rates of A: T leads to G: C transition induced in each of the various sites by these mutagens and those of G: C leads to A: T. 5-Bromouracil induces transitions from G: C to A: T more readily than from A: T to G: C. With 5BU-induced mutation, there is no correlation between the rates of G: C leads to A: T transitions and those of A: T leads to G: C. In UAA sites, all three adenine:thymidine paris respond to 2AP mutagenesis in a similar pattern, In each position in the triplet, response to 2 AP is correlated with that to 5BU. In UGA sites, there are correlations among the spontaneous as well as the 2AP-, HA- and NTG-induced transition rates. 5BU-induced transition rates are usually not correlated with those induced by other mutagens or with the sponatneous ones.

2-Aminopurine↗
PubMed1976

Marker effects on reversion of T4rII mutants.

The frequencies of 2-aminopurine- and 5-bromouracil-induced A:T leads to G:C transitions were compared at nonsense sites throughout the rII region of bacteriophage T4. These frequencies are influenced both by adjacent base pairs within the nonsense codons and by extracodonic factors. Following 2AP treatment, they are high in amber (UAG) and lower in opal (UGA) codons than in allelic ochre (UAA) codons. In general, 5BU-induced transitions are more frequent in both amber and opal codons than in the allelic ochre codons. 2AP- and 5BU-induced transition frequencies in the first and third positions of opal codons are correlated with those in the corresponding positions of the allelic ochre codons. Similarly, the frequencies of 2AP-induced transition in the first and second positions of amber codons and their ochre alleles are correlated. However, there is little correlation between the frequencies of 5BU-induced transitions in the first and second positions of allelic amber and ochre codons.

2-Aminopurine↗
PubMed1974

Bacillus subtilis DNA polymerase III is required for the replication of the virulent bacteriophage phi e.

The virulent phage phie of Bacillus subtilis which contains hydroxymethyluracil in its DNA requires host DNA polymerase III for its DNA replication. DNA polymerase III(ts) mutant cells infected with phie at restrictive temperatures do not support phage DNA synthesis. However, phie grows normally both at low and high temperatures in the mutant's parent strain and in spontaneous DNA polymerase III(+) revertants isolated from the mutant strain. Temperature-shift-down experiments with phie-infected cells having thermosensitive DNA polymerase III (pol III(ts)) indicate that at 48 C the thermolabile DNA polymerase III is irreversibly inactivated and has to be synthesized de novo after the shift to 37 C, before phage DNA synthesis can begin. Temperature-shift-up experiments with phie-infected mutant cells show that phage replication is arrested immediately after the temperature shift and indicate that phie requires DNA polymerase III throughout its replication stage.

Bacillus subtilis↗
PubMed1971

Temperature sensitivity of maltose utilization and lambda resistance in Escherichia coli B.

Escherichia coli B strains that have acquired the malB region from E. coli K-12 are able to utilize maltose and to adsorb phage lambda when grown at 30 C, but when grown at 40 C they do not absorb phage lambda and are devoid of amylomaltase activity. These Mal(ts) Lam(ts) cells can be mutated or transduced to become able to grow on maltose at 40 C, but they still have no detectable amylomaltase activity nor functional lambda receptors at that temperature. This Mal(40) phenotype is governed by a gene located near or at malA. It is suggested that the temperature sensitivity of both characters results from a defect in malT. However, transduction of malA from E. coli B to E. coli K-12 results in a wild-type phenotype, whereas E. coli B cells that have acquired malA from E. coli K-12 donors are still temperature sensitive for both amylomaltase and lambda-receptor production.

Coliphages↗
PubMed1969

Leakiness of pleiotropic maltose-negative, bacteriophage lambda-resistant mutants of Escherichi coli K-12.

Cultures of Escherichia coli K-12 malA(-)lambda(r)gal(-) can be transduced to gal(+) by bacteriophage lambdadg because of leakiness of the lambda(r) phenotype. The efficiency of such transduction is about 10(-5) that of transduction of mal(+)lambda(s) bacteria. Leaky cells (lambda(s)phenocopies) adsorb only very few phage particles, and many transductants, therefore, are defective heterogenotes or show integration of the gal(+) gene, which is unaccompanied by lysogenization.

Bacteriophages↗
PubMed1969

Inactivation of bacteriophage lambda containing semiconserved alkylated deoxyribonucleic acid.

Immediate and delayed inactivation of ethylmethane sulfonate (EMS)-treated lambda phage were studied. Phage particles with one alkylated and one intact deoxyribonucleic acid (DNA) strand were obtained by allowing host-modified, EMS-treated phage to undergo one growth cycle in a nonmodifying host and selecting the progeny with semiconserved parental DNA on a restricting host. The results indicate that particles with one alkylated DNA strand are more sensitive to a second treatment with the alkylating agent. When incubated at 37 C, they are subject to inactivation at a rate which is smaller than that of phages containing two alkylated DNA strands. It appears that depurination events in one of the DNA strands of a phage particle are sufficient to cause death.

Alkylating Agents↗