Showing papers on "Lambda phage published in 1969"
TL;DR: It is concluded that in a Rec(+) strain, the recA(+) product acts to inhibit DNA breakdown determined by the recC(+) and recB(+) products.
Abstract: Strains of Escherichia coli have been made carrying lesions in more than one gene determining recombination. The following genotypes were constructed and verified: recC22 recB21 recA(+), recC22 recB21 recA13, recC22 recB(+)recA13, and recC(+)recB21 recA13. All multiple rec(-) strains carrying recA13 were similar to AB2463, which carries recA13 alone, in their UV sensitivities, recombination deficiencies, and inabilities to induce lambda phage in a lysogen. However, whereas AB2463 shows a high rate of ultraviolet (UV)-induced deoxyribonucleic acid (DNA) breakdown, the multiple rec(-) strains showed the low level characteristic of strains carrying recC22 or recB21 alone. The strain carrying both recC22 and recB21 was similar in all properties to the single mutants, suggesting that both gene products act in the same part of the recombination and UV repair pathways. It is concluded that in a Rec(+) strain, the recA(+) product acts to inhibit DNA breakdown determined by the recC(+) and recB(+) products.
276 citations
TL;DR: A promoter mutation, lambda c17, changes the rate of reading of lambda phage DNA by the RNA polymerase in vitro.
Abstract: A promoter mutation, lambda c17, changes the rate of reading of lambda phage DNA by the RNA polymerase in vitro.
36 citations
34 citations
TL;DR: It is concluded that indirect induction results from the transfer of a UV-damaged colI factor, which leads to inhibition of division of these cells resulting in filament formation, but has little if any effect on cellular DNA replication.
Abstract: Induction of prophage λ in a lysogenic recipient cell may be brought about by mating with ultraviolet irradiated donor cells carrying a transmissible plasmid such as colI (indirect induction). Doses of irradiation to the colI donor required to bring about indirect induction of lysogenic recipient cells reduce to an undetectable level the transfer of viable colI factors to non-lysogenic cells. It is shown by autoradiography that this irradiation does not significantly affect the frequency or amount of colI DNA transfer. Nalidixic acid prevents transfer of colI DNA and also prevents indirect induction. It is concluded that indirect induction results from the transfer of a UV-damaged colI factor. Transfer of the radiation-damaged colI factor to non-lysogenic cells leads to inhibition of division of these cells resulting in filament formation, but has little if any effect on cellular DNA replication.
25 citations
TL;DR: Weak-virulent mutants of temperate coli-phage λ were isolated which can grow on the λCIts lysogen producing a temperature-sensitive repressor but which cannot grow on a wild type λLysogen, producing a normal repressor as discussed by the authors.
Abstract: Weak-virulent mutants of temperate coli-phage λ were isolated which can grow on the λCIts lysogen producing a temperature-sensitive repressor but which cannot grow on the wild type λ lysogen producing a normal repressor. Genetic analysis on the mutants shows that their weak-virulence is attributable to two mutations, one (virL) in the region between sus N213 and c
47 and the other (virR) in the region between c
1 and sus O8. Both mutations are located within the region of non-homology between λ and λimm
434 phages. True virulent mutants which can grow on the wild type λ lysogen can be obtained easily from the weak-virulent mutant by an additional mutation, virC in a region very close to virR. The virulent mutants obtained are similar to the classical λvir mutant (Jacob and Wollman, 1954). The virL and virR mutations are probably operator mutations which render the genome insensitive to the λ repressor.
25 citations
Journal Article•
10 citations
TL;DR: It has been concluded that cysteamine protects the phage against lesions of a type which can be repaired by the bacterial DNA-repair systems.
Abstract: Phage λ, irradiated with ultraviolet light in the presence and absence of the free-radical scavenger and proton donor, cysteamine, have been assayed on normal and DNA-repair deficient bacteria. It has, been concluded that cysteamine protects the phage against lesions of a type which can be repaired by the bacterial DNA-repair systems. Presumably, these are pyrimidine dimers. © 1969 Springer-Verlag.
10 citations
TL;DR: In this paper, the authors show that the phage λ, in which thymine has been totally substituted by the analog, 5-bromouracil, have been irradiated with near visible light in the presence and absence of cysteamine, a free radical scavenger and proton donor.
Abstract: Phage λ, in which thymine has been totally substituted by the analog, 5-bromouracil, have been irradiated with near visible light in the presence and absence of cysteamine, a free radical scavenger and proton donor. These phage were then assayed on normal bacteria and on mutants which are unable to repair DNA lesions. It is concluded that these phage suffer three different kinds of lesions: (1) a class which are not reparable, but which can prevented cysteamine, suggesting that they are sugar damages; (2) a class which are reparable but are not eliminated by cysteamine and (3) a class which can be neither eliminated nor repaired. The nature of the latter two types of lesions cannot be surmised at present.
9 citations
TL;DR: Phage λ, in which thymine has been totally substituted by the analog, 5-bromouracil, have been irradiated with near visible light in the presence and absence of cysteamine, a free radical scavenger and proton donor, and suffer three different kinds of lesions.
Abstract: Phage λ, in which thymine has been totally substituted by the analog, 5-bromouracil, have been irradiated with near visible light in the presence and absence of cysteamine, a free radical scavenger and proton donor. These phage were then assayed on normal bacteria and on mutants which are unable to repair DNA lesions. It is concluded that these phage suffer three different kinds of lesions: (1) a class which are not reparable, but which can prevented cysteamine, suggesting that they are sugar damages; (2) a class which are reparable but are not eliminated by cysteamine and (3) a class which can be neither eliminated nor repaired. The nature of the latter two types of lesions cannot be surmised at present. © 1969 Springer-Verlag.
6 citations
6 citations
Journal Article•
TL;DR: It was concluded that λ· K cannot cooperatively infect E. coli K by λ · C, and it appeared that this fraction was composed of those cells which could support phage growth when singly infected withλ · K.
TL;DR: It appears that depurination events in one of the DNA strands of a phage particle are sufficient to cause death.
Abstract: 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.