Requirement of homologous recombination functions for viability of the Escherichia coli cell that lacks RNase HI and exonuclease V activities

Kogoma, Tokio; Hong, Xiankang; Cadwell, Gregory W.; Barnard, K G; Asai, Tomohisa

doi:10.1016/0300-9084(93)90029-r

Cited by 53 publications

(65 citation statements)

References 43 publications

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“…RecA may bind to the displaced single-stranded DNA in the Rloops. Consistent with this idea, an rnhA mutant, lacking the RNase H1 activity and thus defective in resolving R-loops, chronically induces the SOS response, and RecG protein can also resolve the R-loops in an ATP-dependent manner (Kogoma et al, 1993;Vincent et al, 1996;Fukuoh et al, 1997).…”

Section: Discussionmentioning

confidence: 72%

Roles of the recG gene product of Escherichia coli in recombination repair: Effects of the .DELTA.recG mutation on cell division and chromosome partition.

1997

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The products of the recG and ruvAB genes of Escherichia coli are both thought to promote branch migration of Holliday recombination intermediates by their junction specific helicase activities in homologous recombination and recombination repair. To investigate the in vivo role of the recG gene, we examined the effects of a recG null mutation on cell division and chromosome partition. After UV irradiation at a low dose (5J/ m 2 ), ∆recG mutant formed filamentous cells with unpartitioned chromosomes. A mutation in the sfiA gene, which encodes an SOS-inducible inhibitor of septum formation, partially suppressed filamentation of recG mutant cells, but did not prevent the formation of anucleate cells. The sensitivity to UV light and the cytological phenotypes after UV irradiation of a recA recG double mutant were similar to a recA single mutant, consistent with the role of recG, which is assigned to a later stage in recombination repair than recA. The recG ruvAB and recG ruvC double mutants were more sensitive to UV, almost as sensitive as the recA mutant and showed more extreme phenotypes concerning filamentation and chromosome nondisjunction, both after UV irradiation and without UV irradiation than either recG or ruv single mutants. The recG polA12 (Ts) mutant, which is temperature sensitive in growth, formed filamentous cells with centrally located chromosome aggregates when grown at nonpermissive temperature similar to the UV irradiated recG mutant. These results support the notion that RecG is involved in processing Holliday intermediates in recombination repair in vivo. We suggest that the defect in the processing in the recG mutant results in accumulation of nonpartitioned chromosomes, which are linked by Holliday junctions.

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Section: Discussionmentioning

confidence: 72%

Roles of the recG gene product of Escherichia coli in recombination repair: Effects of the .DELTA.recG mutation on cell division and chromosome partition.

1997

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“…The sequence revealed that rnhA224 is a UGA nonsense mutation which could be leaky in certain genetic backgrounds. Although both rnhA224(UGA) and rnhA (Null)::cat mutants have RNase HI activities at levels below the detection limit (8) (12). Therefore, the possibility that the residual level of activity may have been sufficient for the requirement for oriC function has been raised.…”

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confidence: 99%

“…AQ8065 was constructed by introducing the recB21 mutation [rnhA::cat recB(Ts,] (O and 0) were grown for about three generations to 2 x 10 cells per ml in CAA medium (12) containing [3H]thymidine (5 ,Ci; 10 p.g/ml) and 2'-deoxyadenosine (300 ,ug/ml). Cells were then collected by filtration, washed, and resuspended in fresh medium.…”

mentioning

confidence: 99%

“…Samples were taken at intervals, and the copy number of pOC81 was determined by Southern blot hybridization as described previously (17). The probe was the BamHI-BamHI fragment of pNK862 (23) (12). This strain pOC81 is a minichromosome which carries the oriC site and was very sensitive to L broth but could grow relatively well in thus is capable of autonomous replication.…”

mentioning

confidence: 99%

“…This strain pOC81 is a minichromosome which carries the oriC site and was very sensitive to L broth but could grow relatively well in thus is capable of autonomous replication. This plasmid transminimal medium supplemented with Casamino Acids (12).…”

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confidence: 99%

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Absence of a direct role for RNase HI in initiation of DNA replication at the oriC site on the Escherichia coli chromosome

Hong

Kogoma

1993

J Bacteriol

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On the basis of the experiments carried out with rnhA224 mutants, we previously concluded that RNase HI is not essential for initiation of Escherichia coli chromosome replication at oriC (T. Kogoma, N.L. Subia, and K. von Meyenburg, Mol. Gen. Genet. 200:103-109, 1985). In light of the recent finding that rnhA224 is a UGA nonsense mutation which can be leaky in certain genetic backgrounds, we reexamined this conclusion with the use of rnhA339 (Null)::cat mutants. The possibility that recB+ is required for initiation at the alternative origins (oriKs) of replication in rnhA mutants was also tested. The results clearly indicated that RNase HI is not essential for oriC initiation and that recB+ is not required for initiation at oriK sites.

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Homologous recombination-dependent initiation of DNA replication from DNA damage-inducible origins in Escherichia coli.

et al. 1993

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Escherichia coli cells induced for the SOS response express inducible stable DNA replication (iSDR) as an SOS function. Initiation of iSDR is independent of transcription, translation and DnaA protein, which are essential for initiation of DNA replication from oriC. We found that a recA mutant that is defective in recombination but proficient in SOS induction could not elicit iSDR. In contrast, iSDR was enhanced by recD and recJ mutations that inactivate the exonuclease V activity of the RecBCD enzyme and the RecJ exonuclease activity, respectively. A mutation in the ruvC gene that blocks the resolution of recombination intermediates (i.e. Holliday structures) also enhanced iSDR. Furthermore, inhibition of branch migration by recG or ruvAB mutations dramatically increased the iSDR activity. recBC mutants are defective in iSDR induction but the defect was suppressed by a mutation in the sbcA gene. The major product of minichromosomes replicated by iSDR was covalently closed circular monomers. We propose that recombination intermediates (i.e. D‐loop structures) created by the action of RecA recombinase and RecBC(D) helicase play a central role in initiation of iSDR.

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Requirement of homologous recombination functions for viability of the Escherichia coli cell that lacks RNase HI and exonuclease V activities

Cited by 53 publications

References 43 publications

Roles of the recG gene product of Escherichia coli in recombination repair: Effects of the .DELTA.recG mutation on cell division and chromosome partition.

Roles of the recG gene product of Escherichia coli in recombination repair: Effects of the .DELTA.recG mutation on cell division and chromosome partition.

Absence of a direct role for RNase HI in initiation of DNA replication at the oriC site on the Escherichia coli chromosome

Homologous recombination-dependent initiation of DNA replication from DNA damage-inducible origins in Escherichia coli.

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