Additive Effects of SbcCD and PolX Deficiencies in the In Vivo Repair of DNA Double-Strand Breaks in<i>Deinococcus radiodurans</i>

Bentchikou, Esma; Servant, Pascale; Coste, Geneviève; Sommer, Suzanne

doi:10.1128/jb.00452-07

Cited by 51 publications

(40 citation statements)

References 47 publications

(46 reference statements)

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“…Homologs of Rad50/SbcC (DR1922) and Mre11/SbcD (DR1921) do not seem crucial for the recombinational repair of DSBs in D. radiodurans. The sbcCD mutant cells are resistant to doses as high as 10 kGy and exhibit only a slight delay in the reconstitution of the radiation-fragmented genome (48) (Fig. 8).…”

Section: Recombinational Processes In D Radiodurans Dna Repairmentioning

confidence: 99%

“…Another nuclease, DR0505, can act on hairpin structures as an ATP-dependent ssDNA-dsDNA junction endonuclease (318). While individual deletions of SbcCD, Pol X, and DR0505 have no effects on DNA damage sensitivity, a coupled SbcCD-Pol X deficiency in D. radiodurans yields an additive radiation-sensitive phenotype and an additive delay in genome reconstitution (48,318,343 (456) unique to the Deinococcaceae (216). PprA is highly expressed after ionizing radiation and desiccation (368,602) and repressed by LexA2 (537), PprM (468), and RecX (563).…”

Section: Recombinational Processes In D Radiodurans Dna Repairmentioning

confidence: 99%

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Oxidative Stress Resistance inDeinococcus radiodurans

Slade

Radman

2011

Microbiol Mol Biol Rev

659

639

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SUMMARY Deinococcus radiodurans is a robust bacterium best known for its capacity to repair massive DNA damage efficiently and accurately. It is extremely resistant to many DNA-damaging agents, including ionizing radiation and UV radiation (100 to 295 nm), desiccation, and mitomycin C, which induce oxidative damage not only to DNA but also to all cellular macromolecules via the production of reactive oxygen species. The extreme resilience of D. radiodurans to oxidative stress is imparted synergistically by an efficient protection of proteins against oxidative stress and an efficient DNA repair mechanism, enhanced by functional redundancies in both systems. D. radiodurans assets for the prevention of and recovery from oxidative stress are extensively reviewed here. Radiation- and desiccation-resistant bacteria such as D. radiodurans have substantially lower protein oxidation levels than do sensitive bacteria but have similar yields of DNA double-strand breaks. These findings challenge the concept of DNA as the primary target of radiation toxicity while advancing protein damage, and the protection of proteins against oxidative damage, as a new paradigm of radiation toxicity and survival. The protection of DNA repair and other proteins against oxidative damage is imparted by enzymatic and nonenzymatic antioxidant defense systems dominated by divalent manganese complexes. Given that oxidative stress caused by the accumulation of reactive oxygen species is associated with aging and cancer, a comprehensive outlook on D. radiodurans strategies of combating oxidative stress may open new avenues for antiaging and anticancer treatments. The study of the antioxidation protection in D. radiodurans is therefore of considerable potential interest for medicine and public health.

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Section: Recombinational Processes In D Radiodurans Dna Repairmentioning

confidence: 99%

Section: Recombinational Processes In D Radiodurans Dna Repairmentioning

confidence: 99%

Oxidative Stress Resistance inDeinococcus radiodurans

Slade

Radman

2011

Microbiol Mol Biol Rev

659

639

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“…Orthologues of SbcC and SbcD are present in many organisms from all three kingdoms of life (Sharples & Leach, 1995), including A. baylyi (Barbe et al, 2004). In the E. coli wild-type background, sbcC or sbcD mutations have no strong phenotype, whereas in Deinococcus radiodurans they cause reduced survival after gamma irradiation (Bentchikou et al, 2007). In Bacillus subtilis, the SbcCD complex is involved in DNA repair and is then mostly colocalized with the replication machinery (Mascarenhas et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

The RecBCD and SbcCD DNases suppress homology-facilitated illegitimate recombination during natural transformation of Acinetobacter baylyi

Harms

Wackernagel

2008

Microbiology

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During natural transformation of Acinetobacter baylyi, the genomic integration of foreign (nonhomologous) DNA is possible when the DNA contains a single segment homologous to the recipient genome (anchor) through homologous recombination in the anchor facilitating illegitimate recombination in the neighbouring foreign DNA (homology-facilitated illegitimate recombination; HFIR). DNA integration by HFIR occurs about 10 000 times less frequently than fully homologous recombination, but at least 100 000-fold more frequently than integration in the absence of any homology. We investigated the influence of the RecBCD enzyme (DNase/ helicase) and SbcCD DNase (DNA-structure-specific single-strand endonuclease and exonuclease) on HFIR. In a recBCD null mutant the acquisition of foreign DNA was elevated 11-fold relative to wild-type cells by a 6.9-fold increased HFIR frequency and by the integration of longer stretches of foreign DNA in each event. In an sbcCD null mutant, the foreign DNA acquisition was 4.5-fold higher than in the wild-type, while homologous transformation with large DNA molecules was unaffected and increased 3.2-fold with small DNA fragments. The sbcCD mutation partially suppressed the high UV sensitivity and low viability of the recBCD mutant and also decreased its foreign DNA acquisition by HFIR to the lower level of the sbcCD mutant. We propose that suppression of HFIR results from the elimination of double-stranded intermediates of the HFIR process during transformation by RecBCD, and by SbcCD interfering with branched molecules. Our results provide evidence that the homologous recombination enzymes RecBCD and SbcCD control the level of foreign DNA acquisition by HFIR.

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“…In Bacillus subtilis and Deinococcus radiodurans, the deletion of sbcC results in an increased sensitivity of the cells to ionizing radiation (28). Deletions of sbcC and/or sbcD in D. radiodurans also result in delayed repair kinetics of DNA DSBs following ␥ irradiation (5).…”

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confidence: 99%

Rad50 Is Not Essential for the Mre11-Dependent Repair of DNA Double-Strand Breaks inHalobacteriumsp. Strain NRC-1

Kish

DiRuggiero

2008

J Bacteriol

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The genome of the halophilic archaeon Halobacterium sp. strain NRC-1 encodes homologs of the eukaryotic Mre11 and Rad50 proteins, which are involved in the recognition and end processing of DNA double-strand breaks in the homologous recombination repair pathway. We have analyzed the phenotype of Halobacterium deletion mutants lacking mre11 and/or rad50 after exposure to UV-C radiation, an alkylating agent (N-methyl-N-nitro-N-nitrosoguanidine), and ␥ radiation, none of which resulted in a decrease in survival of the mutant strains compared to that of the background strain. However, a decreased rate of repair of DNA double-strand breaks in strains lacking the mre11 gene was observed using pulsed-field gel electrophoresis. These observations led to the hypothesis that Mre11 is essential for the repair of DNA double-strand breaks in Halobacterium, whereas Rad50 is dispensable. This is the first identification of a Rad50-independent function for the Mre11 protein, and it represents a shift in the Archaea away from the eukaryotic model of homologous recombination repair of DNA double-strand breaks.

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Additive Effects of SbcCD and PolX Deficiencies in the In Vivo Repair of DNA Double-Strand Breaks inDeinococcus radiodurans

Cited by 51 publications

References 47 publications

Oxidative Stress Resistance inDeinococcus radiodurans

Oxidative Stress Resistance inDeinococcus radiodurans

The RecBCD and SbcCD DNases suppress homology-facilitated illegitimate recombination during natural transformation of Acinetobacter baylyi

Rad50 Is Not Essential for the Mre11-Dependent Repair of DNA Double-Strand Breaks inHalobacteriumsp. Strain NRC-1

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