PprA: a novel protein from <i>Deinococcus radiodurans</i> that stimulates DNA ligation

Narumi, Issay; Satoh, Katsuya; Cui, Suzhen; Funayama, Tomoo; Kitayama, Shigeru; Watanabe, Hiroshi

doi:10.1111/j.1365-2958.2004.04272.x

Cited by 147 publications

(144 citation statements)

References 27 publications

(55 reference statements)

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“…8). D. radiodurans PprA preferentially binds to dsDNA carrying strand breaks (Narumi et al, 2004). DNA strand breaks also result from the process of DNA replication.…”

Section: Discussionmentioning

confidence: 99%

“…An unknown protein down-regulated by LexA2 enhances pprA promoter activation. RecA and PprA play crucial roles in recombination and end-joining repairs, respectively (Satoh et al, 2002, Narumi et al, 2004.…”

Section: Discussionmentioning

confidence: 99%

“…The pprA gene encoding the novel radiation-inducible protein PprA plays a critical role in the radioresistance of D. radiodurans (Narumi et al, 2004). To investigate whether LexA homologues are involved in PprA induction, changes in pprA promoter activation following c-irradiation (8 kGy) were compared between parental and disruptant strains using the luciferase reporter assay.…”

Section: Sensitivity Of Gene Disruptant Strains To C-raysmentioning

confidence: 99%

“…Additionally, analysis of DNAdamage-sensitive strains IRS24 (Mattimore et al, 1995) and KH840 (Kitayama & Matsuyama, 1975) identified a novel regulatory protein (DR0167; PprI protein, also called IrrE protein) that plays a role in regulating recA and pprA gene expression following c-irradiation (Earl et al, 2002;Hua et al, 2003;Ohba et al, 2005). Furthermore, in a previous study we identified the radiation-responsive minimal promoter of the pprA gene encoding the novel radiation-inducible protein PprA, which plays a critical role in radioresistance of D. radiodurans (Narumi et al, 2004;Ohba et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

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Down-regulation of radioresistance by LexA2 in Deinococcus radiodurans

et al. 2006

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The extremely radioresistant bacterium Deinococcus radiodurans contains two LexA homologues (LexA1 and LexA2) that are possible transcriptional regulators associated with the DNA damage response. In this study, resequencing revealed that there was an additional cytosine nucleotide (nucleotide position 612) in the D. radiodurans lexA2 gene. Purified LexA2 possessed proteolytic activity that could be stimulated by RecA. In an effort to gain an insight into the role of LexA2 in the radiation response mechanism, recA, lexA1 and lexA2 disruptant strains were generated and investigated. The intracellular level of RecA increased in lexA1 and lexA2 disruptant strains following γ-irradiation as in the wild-type strain. These results indicated that the two LexA homologues did not possess functional overlap regarding the induction of RecA. The lexA2 disruptant strains exhibited a much higher resistance to γ-rays than the wild-type strain. Furthermore, a luciferase assay showed that pprA promoter activation was enhanced in the lexA2 disruptant strain following γ-irradiation. The pprA gene encoding the novel radiation-inducible protein PprA plays a critical role in the radioresistance of D. radiodurans. The increase in radioresistance of the lexA2 disruptant strain is explained in part by the enhancement of pprA promoter activation.

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“…8). D. radiodurans PprA preferentially binds to dsDNA carrying strand breaks (Narumi et al, 2004). DNA strand breaks also result from the process of DNA replication.…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Sensitivity Of Gene Disruptant Strains To C-raysmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Down-regulation of radioresistance by LexA2 in Deinococcus radiodurans

et al. 2006

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“…The products of additional genes specifically conserved in Deinococcus are also involved in DNA repair and radiation tolerance. These include PprA (reported to stimulate ligase activity) (Narumi et al, 2004), DdrA (an oligomeric ring-forming protein involved in DNA extremity protection) (Harris et al, 2004;Gutsche et al, 2008), DdrB, DdrC and DdrD (functions unknown) de Groot et al, 2009) and IrrE (regulator of recA and pprA expression) (Earl et al, 2002a;Hua et al, 2003;Lu et al, 2009;Vujicic-Zagar et al, 2009). Homologues of DNA repair photolyases and specialized translesion synthesis (TLS) DNA polymerases have not been identified in D. radiodurans and D. geothermalis.…”

Section: Introductionmentioning

confidence: 99%

Mutagenic lesion bypass and two functionally different RecA proteins in Deinococcus deserti

Dulermo

Fochesato

Blanchard

et al. 2009

Molecular Microbiology

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SummaryRecA is essential for extreme radiation tolerance in Deinococcus radiodurans. Interestingly, Sahara bacterium Deinococcus deserti has three recA genes (recAC, recAP1, recAP3) that code for two different RecA proteins (RecAC, RecAP). Moreover, and in contrast to other sequenced Deinococcus species, D. deserti possesses homologues of translesion synthesis (TLS) DNA polymerases, including ImuY and DnaE2. Together with a lexA homologue, imuY and dnaE2 form a gene cluster similar to a widespread RecA/LexA-controlled mutagenesis cassette. After having developed genetic tools, we have constructed mutant strains to characterize these recA and TLS polymerase genes in D. deserti. Both RecAC and RecAP are functional and allow D. deserti to survive, and thus repair massive DNA damage, after exposure to high doses of radiation. D. deserti is mutable by UV, which requires ImuY, DnaE2 and RecAC, but not RecAP. RecAC, but not RecAP, facilitates induced expression of imuY and dnaE2 following UV exposure. We propose that the extra recAP1 and recAP3 genes may provide higher levels of RecA protein for efficient error-free repair of DNA damage, without further increasing error-prone lesion bypass by ImuY and DnaE2, whereas limited TLS may contribute to adaptation to harsh conditions by generating genetic variability.

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DNA Double‐strand Breaks and Their Consequences in Bacteria

Kobayashi

Handa

2009

Encyclopedia of Life Sciences

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Deoxyribonucleic acid (DNA) double‐strand breaks, which are caused by many factors such as chemical treatments, radiations and, often, biological factors, are lethal events in organisms carrying DNA as their genome include bacteria. There are various mechanisms that work, sometimes in collaboration or competition with each other, in the processing of these breaks. These include exonucleolytic degradation, end joining and recombination repair. These may bring about death, restoration or recombinational/mutational changes in the genome. Intragenomic collaboration and conflict between various pathways can be a force in their genome evolution. Recent analyses suggest that DNA double‐strand breaks switch on the programme of cell death in bacteria. DNA double‐strand breakage and its consequences in bacteria may provide a good model system to analyse the dynamic relationship between life, death and evolution. Understanding these processes in bacteria is important in medicine, environmental studies and industrial application. Key concepts: DNA double‐strand breakage and its consequences in bacteria may provide a model system to analyse the relationship between life, death and evolution. DNA double‐strand breakage may switch on programmes of cell death in bacteria.

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PprA: a novel protein from Deinococcus radiodurans that stimulates DNA ligation

Cited by 147 publications

References 27 publications

Down-regulation of radioresistance by LexA2 in Deinococcus radiodurans

Down-regulation of radioresistance by LexA2 in Deinococcus radiodurans

Mutagenic lesion bypass and two functionally different RecA proteins in Deinococcus deserti

DNA Double‐strand Breaks and Their Consequences in Bacteria

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