Repair of X-Ray Damage to the Deoxyribonucleic Acid in Micrococcus radiodurans

Dean, C.J.; Feldschreiber, P.; Lett, J. T.

doi:10.1038/209049a0

Cited by 153 publications

(41 citation statements)

References 19 publications

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“…To measure DNA synthesis at short times after irradiation we used initially unlabelled bacteria, so that small amounts of synthesis would give relatively large increases in radioactive counts (Setlow & Setlow, 1970). The results confirmed previous findings that there is a delay in DNA synthesis which is linearly related to the radiation dose (Setlow & Boling, 1965;Dean, Feldschreiber & Lett, 1966). Under comparable conditions to those used to measure the rate of recombination repair the delay was 1.0 min per 5.6 x I O -~ J mm-2 U.V.…”

Section: Recombination Repair Rates 257supporting

confidence: 80%

The Rate of Recombination Repair and its Relationship to the Radiation-induced Delay in DNA Synthesis in Micrococcus radiodurans

Moseley

Copland

1976

Journal of General Microbiology

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SUMMARYThe measurement of the time at which normal colony-forming ability returns in irradiated cultures of Micrococcus radiodurans tsI held at 30 "C can be used to estimate the time of completion of recombination repair. By comparing the times to complete such repair in populations given increasing radiation doses it is possible to calculate the rate of recombination repair. The rate was independent of the radiation dose; recombination could repair in one minute the damage caused either by 1.2 krad gamma radiation or 4 x I O -~ J mm-2 U.V. radiation.The time taken for the normal rate of DNA synthesis to return in irradiated M. radiodurans tsr was measured under conditions identical to those used to measure recombination repair. The delay in DNA synthesis was 1.0 min per 1 -2 krad gamma radiation and 1-0 min per 5-6 x I O -~ J mm-2 U.V. radiation. The data suggest that the normal rate of DNA synthesis resumes immediately after the completion of recombination repair of gamma-induced damage, but before the completion of recombination repair of u.v.-induced damage. It is postulated that cell death at the lethal dose of U.V. radiation is caused by a second round of replication of DNA which is still being repaired by recombination.

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Section: Recombination Repair Rates 257supporting

confidence: 80%

The Rate of Recombination Repair and its Relationship to the Radiation-induced Delay in DNA Synthesis in Micrococcus radiodurans

Moseley

Copland

1976

Journal of General Microbiology

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“…The 1-kb DNA ladder was composed of 10 DNA fragments (1,2,3,4,5,6,7,8,9, and 10 kbp; Takara Bio). The 100-bp DNA ladder (Takara Bio) was composed of 11 DNA fragments (0.…”

Section: Methodsmentioning

confidence: 99%

“…3 Ionizing irradiation and desiccation cause DNA double-strand breaks (DSBs) 9,10 ; thus, they are lethal to nearly all organisms. D. radiodurans can, however, survive >100 DSBs in their genomic DNA by irradiation with 5000 Gy, 11 whereas E. coli cannot live with only a few DSBs.…”

Section: Introductionmentioning

confidence: 99%

Interaction of double‐stranded DNA with polymerized PprA protein from Deinococcus radiodurans

et al. 2014

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Pleiotropic protein promoting DNA repair A (PprA) is a key protein that facilitates the extreme radioresistance of Deinococcus radiodurans. To clarify the role of PprA in the radioresistance mechanism, the interaction between recombinant PprA expressed in Escherichia coli with several double-stranded DNAs (i.e., super coiled, linear, or nicked circular dsDNA) was investigated. In a gel-shift assay, the band shift of supercoiled pUC19 DNA caused by the binding of PprA showed a bimodal distribution, which was promoted by the addition of 1 mM Mg, Ca, or Sr ions. The dissociation constant of the PprA-supercoiled pUC19 DNA complex, calculated from the relative portions of shifted bands, was 0.6 lM with Hill coefficient of 3.3 in the presence of 1 mM Mg acetate. This indicates that at least 281 PprA molecules are required to saturate a supercoiled pUC19 DNA, which is consistent with the number (280) of bound PprA molecules estimated by the UV absorption of the PprA-pUC19 complex purified by gel filtration. This saturation also suggests linear polymerization of PprA along the dsDNA. On the other hand, the bands of linear dsDNA and nicked circular dsDNA that eventually formed PprA complexes did not saturate, but created larger molecular complexes when the PprA concentration was >1.3 lM. This result implies that DNAbound PprA aids association of the termini of damaged DNAs, which is regulated by the concentration of PprA. These findings are important for the understanding of the mechanism underlying effective DNA repair involving PprA.

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“…This resistance has been attributed to its highly proficient DNA repair capacity (Battista, 1997;Narumi, 2003;Cox & Battista, 2005). The most noteworthy characteristic of D. radiodurans is its capacity for repairing DNA double-strand breaks induced by ionizing radiation (Dean et al, 1966;Kitayama & Matsuyama, 1968;Grimsley et al, 1991). The highly efficient double-strand break repair process in D. radiodurans is radiation-inducible and is dependent on de novo protein synthesis following irradiation (Kitayama & Matsuyama, 1971).…”

Section: Introductionmentioning

confidence: 99%

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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Repair of X-Ray Damage to the Deoxyribonucleic Acid in Micrococcus radiodurans

Cited by 153 publications

References 19 publications

The Rate of Recombination Repair and its Relationship to the Radiation-induced Delay in DNA Synthesis in Micrococcus radiodurans

The Rate of Recombination Repair and its Relationship to the Radiation-induced Delay in DNA Synthesis in Micrococcus radiodurans

Interaction of double‐stranded DNA with polymerized PprA protein from Deinococcus radiodurans

Down-regulation of radioresistance by LexA2 in Deinococcus radiodurans

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