Thymineless death in Escherichia coli dnaB mutants and in a dnaB dnaG double mutant

Sicard, N; Bouvier, F

doi:10.1128/jb.132.3.779-783.1977

Cited by 3 publications

(1 citation statement)

References 20 publications

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“…According to this hypothesis, failure to detect chromosomeless cell formation during inhibition of DNA replication, e.g., during thymine starvation of E. coli recA +, could be due to an alteration in transcriptional fidelity (and subsequent loss of cell viability) before the divisions took place, rather than the production of a specific negative effector of division (or a need for chromosome replication). It is noteworthy in this regard that a number of the mutants which were capable of continued division during inhibition of DNA synthesis were also relatively resistant to loss of colony-forming ability (2,19,25,45) or continued to grow for extended periods of time (20,21,41). Sargent (41) has shown that chromosomeless cell formation in B. subtilis occurs primarily in those situations in which mass increase continues extensively in the absence of DNA replication.…”

Section: Resultsmentioning

confidence: 99%

Coordination between chromosome replication and cell division in Escherichia coli

Tang¹,

Helmstetter²

1980

J Bacteriol

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Cell division properties of Escherichia coli B/r containing either a dnaC or a dnaI mutation were examined. Incubation at nonpermissive temperature resulted in the eventual production of celLs of approximately normal size, or slightly smaller, which lacked chromosomal DNA. The cell division patterns in cultures which were grown at permissive temperature and then shifted to nonpermissive temperature were consistent with: first, division and equipartition ofchromosomes by cells which were in the C and D periods at the time of the shift; second, an apparent delay in cell division; and third, commencement of the formation of chromosomeless cells. In glucose-grown cultures of the dnaI mutant, production of chromosomeless cells continued for at least 120 min, whereas in the dnaC mutant chromosomeless cells were forned during a single interval between 110 and 130 min after the temperature shift. The results are discussed in light of the hypothesis that replication of a specific chromosomal region is not an obligatory requirement for the initiation and completion of the processes leading to division in a cell which contains at least one functioning chromosome. 1148 on August 1, 2020 by guest

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Section: Resultsmentioning

confidence: 99%

Coordination between chromosome replication and cell division in Escherichia coli

Tang¹,

Helmstetter²

1980

J Bacteriol

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Recombination-deficient mutations and thymineless death in Escherichia coli K12: reciprocal effects of recBC and recF and indifference of recA mutations

Nakayama¹,

Nakayama²,

Nakayama³

et al. 1982

Can. J. Microbiol.

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In an approach to characterizing the nature of the lethal event in thymineless death (TLD), rec mutants of Escherichia coli K12 were examined for their sensitivity to TLD. The recB21 and recC22 mutations sensitized cells of the AB1157 line to TLD but not cells of the HF4733 line. This increased sensitivity was not suppressed substantially by either sbcB15 or xonA1 mutation. In contrast, a recF mutation appeared to make cells more resistant to TLD than rec+ cells. Three different recA alleles were shown not to affect TLD appreciably. These results not only provide further support for the view that the site of the lethal event in TLD is cellular DNA, but also strongly suggest the involvement of the recBC and recF gene products in TLD. The apparent indifference of recA mutation implies that the conventional recombination and repair pathways per se are not involved in TLD and that the hypothetical lethal damage to DNA may be unique in nature.

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Thymine Metabolism and Thymineless Death in Prokaryotes and Eukaryotes

Ahmad

Kirk²,

Eisenstark³

1998

Annu. Rev. Microbiol.

216

228

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For many years it has been known that thymine auxotrophic microorganisms undergo cell death in response to thymine starvation [thymineless death (TLD)]. This effect is unusual in that deprivation of many other nutritional requirements has a biostatic, but not lethal, effect. Studies of numerous microbes have indicated that thymine starvation has both direct and indirect effects. The direct effects involve both single- and double-strand DNA breaks. The former may be repaired effectively, but the latter lead to cell death. DNA damaged by thymine starvation is a substrate for DNA repair processes, in particular recombinational repair. Mutations in recBCD recombinational repair genes increase sensitivity to thymineless death, whereas mutations in RecF repair protein genes enhance the recovery process. This suggests that the RecF repair pathway may be critical to cell death, perhaps because it increases the occurrence of double-strand DNA breaks with unique DNA configurations at lesion sites. Indirect effects in bacteria include elimination of plasmids, loss of transforming ability, filamentation, changes in the pool sizes of various nucleotides and nucleosides and in their excretion, and phage induction. Yeast cells show effects similar to those of bacteria upon thymine starvation, although there are some unique features. The mode of action of certain anticancer drugs and antibiotics is based on the interruption of thymidylate metabolism and provides a major impetus for further studies on TLD. There are similarities between TLD of bacteria and death of eukaryotic cells. Also, bacteria have "survival" genes other than thy (thymidylate synthetase), and this raises the question of whether there is a relationship between the two. A model is presented for a molecular basis of TLD.

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Thymineless death in Escherichia coli dnaB mutants and in a dnaB dnaG double mutant

Cited by 3 publications

References 20 publications

Coordination between chromosome replication and cell division in Escherichia coli

Coordination between chromosome replication and cell division in Escherichia coli

Recombination-deficient mutations and thymineless death in Escherichia coli K12: reciprocal effects of recBC and recF and indifference of recA mutations

Thymine Metabolism and Thymineless Death in Prokaryotes and Eukaryotes

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