Inducibility of Lambda Phage Development in Escherichia coli Mutants Thermosensitive for DNA Replication

Abstract In a thermosensitive dnaZ mutant lysogenic for λ, induction of the prophage development was provoked at the restrictive temperature. In dnaD strain, spontaneous release of λ proceeded even at 43 °C, but distinct induction of the prophage development was not caused by a heat treatment. Similarly, shift up of growth temperature did not lead to induction of λ in lysogens carrying thermosensitive mutation in dnaH function or DNA polymerase I. In dnaH mutant, multiplication of λ-virulent phage proceeded normally at 43 °C.

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The mechanism of recA polA lethality: suppression by RecA-independent recombination repair activated by the lexA(Def) mutation in Escherichia coli.

Genetics ◽

10.1093/genetics/139.4.1483 ◽

1995 ◽

Vol 139 (4) ◽

pp. 1483-1494 ◽

Cited By ~ 2

Author(s):

Y Cao ◽

T Kogoma

Keyword(s):

Escherichia Coli ◽

Dna Replication ◽

Dna Polymerase ◽

Reca Protein ◽

Minor Role ◽

Temperature Sensitive ◽

Restrictive Temperature ◽

Dna Polymerase I ◽

Recombination Repair ◽

Polymerase I

Abstract The mechanism of recA polA lethality in Escherichia coli has been studied. Complementation tests have indicated that both the 5'-->3' exonuclease and the polymerization activities of DNA polymerase I are essential for viability in the absence of RecA protein, whereas the viability and DNA replication of DNA polymerase I-defective cells depend on the recombinase activity of RecA. An alkaline sucrose gradient sedimentation analysis has indicated that RecA has only a minor role in Okazaki fragment processing. Double-strand break repair is proposed for the major role of RecA in the absence of DNA polymerase I. The lexA(Def)::Tn5 mutation has previously been shown to suppress the temperature-sensitive growth of recA200(Ts) polA25::spc mutants. The lexA(Def) mutation can alleviate impaired DNA synthesis in the recA200(Ts) polA25::spc mutant cells at the restrictive temperature. recF+ is essential for this suppression pathway. recJ and recQ mutations have minor but significant adverse effects on the suppression. The recA200(Ts) allele in the recA200(Ts) polA25::spc lexA(Def) mutant can be replaced by delta recA, indicating that the lexA(Def)-induced suppression is RecA independent. lexA(Def) reduces the sensitivity of delta recA polA25::spc cells to UV damage by approximately 10(4)-fold. lexA(Def) also restores P1 transduction proficiency to the delta recA polA25::spc mutant to a level that is 7.3% of the recA+ wild type. These results suggest that lexA(Def) activates a RecA-independent, RecF-dependent recombination repair pathway that suppresses the defect in DNA replication in recA polA double mutants.

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Interaction between the plasmid R6K andEscherichia coliwith defective DNA polymerase I

Genetics Research ◽

10.1017/s0016672300018498 ◽

1978 ◽

Vol 32 (1) ◽

pp. 25-35 ◽

Cited By ~ 1

Author(s):

D. J. Tweats ◽

J. T. Smith

Keyword(s):

Cell Division ◽

Dna Polymerase ◽

Temperature Sensitive ◽

Restrictive Temperature ◽

Dna Polymerase I ◽

E Coli ◽

R Factor ◽

Polymerase I

SUMMARYInitial experiments demonstrated that the plasmid R6K cannot be transferred to or maintained readily in theE. coliDNA polymerase I deficient strain JG138polA1. Results withE. coliMM386polA12(R6K), which has a temperature sensitive polymerase I enzyme, showed cell division becomes abnormal when the polymerase I enzyme of the host bacteria is inactivated at the restrictive temperature. Under conditions of polymerase I deficiency, R6K replication, as measured by monitoring R-factor-mediated β-lactamase activity, also becomes abnormal with the loss of multiple R6K copies per cell and the apparent maintenance of a single R-factor copy per cell.

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