scholarly journals Effect of a recD Mutation on DNA Damage Resistance and Transformation in Deinococcus radiodurans

2007 ◽  
Vol 189 (14) ◽  
pp. 5101-5107 ◽  
Author(s):  
Matthew D. Servinsky ◽  
Douglas A. Julin
Keyword(s):  
Hydrogen Peroxide ◽  
Dna Damage ◽  
Ionizing Radiation ◽  
Mitomycin C ◽  
Deinococcus Radiodurans ◽  
Uv Light ◽  
Gene Encoding ◽  
Significant Similarity ◽  
Damage Repair ◽  
Recbcd Enzyme

ABSTRACT The bacterium Deinococcus radiodurans is resistant to extremely high levels of DNA-damaging agents such as UV light, ionizing radiation, and chemicals such as hydrogen peroxide and mitomycin C. The organism is able to repair large numbers of double-strand breaks caused by ionizing radiation, in spite of the lack of the RecBCD enzyme, which is essential for double-strand DNA break repair in Escherichia coli and many other bacteria. The D. radiodurans genome sequence indicates that the organism lacks recB and recC genes, but there is a gene encoding a protein with significant similarity to the RecD protein of E. coli and other bacteria. We have generated D. radiodurans strains with a disruption or deletion of the recD gene. The recD mutants are more sensitive than wild-type cells to irradiation with gamma rays and UV light and to treatment with hydrogen peroxide, but they are not sensitive to treatment with mitomycin C and methyl methanesulfonate. The recD mutants also show greater efficiency of transformation by exogenous homologous DNA. These results are the first indication that the D. radiodurans RecD protein has a role in DNA damage repair and/or homologous recombination in the organism.

scholarly journals The IrrE Protein of Deinococcus radiodurans R1 Is a Novel Regulator of recA Expression

2002 ◽  
Vol 184 (22) ◽  
pp. 6216-6224 ◽  
Author(s):  
Ashlee M. Earl ◽  
Michael M. Mohundro ◽  
I. Saira Mian ◽  
John R. Battista
Keyword(s):  
Dna Damage ◽  
Ionizing Radiation ◽  
Radiation Resistance ◽  
Deinococcus Radiodurans ◽  
Genomic Library ◽  
Uv Light ◽  
Regulatory Protein ◽  
Chromosome I ◽  
Ionizing Radiation Resistance ◽  
Deinococcus Radiodurans R1

ABSTRACT IRS24 is a DNA damage-sensitive strain of Deinococcus radiodurans strain 302 carrying a mutation in an uncharacterized locus designated irrE. Five overlapping cosmids capable of restoring ionizing radiation resistance to IRS24 were isolated from a genomic library. The ends of each cloned insert were sequenced, and these sequences were used to localize irrE to a 970-bp region on chromosome I of D. radiodurans R1. The irrE gene corresponds to coding sequence DR0167 in the R1 genome. The irrE gene encodes a 35,000-Da protein that has no similarity to any previously characterized peptide. The irrE locus of R1 was also inactivated by transposon mutagenesis, and this strain was sensitive to ionizing radiation, UV light, and mitomycin C. Preliminary findings indicate that IrrE is a novel regulatory protein that stimulates transcription of the recA gene following exposure to ionizing radiation.

Analysis of ionizing radiation-induced foci of DNA damage repair proteins

2005 ◽  
Vol 574 (1-2) ◽  
pp. 22-33 ◽  
Author(s):  
Lieneke R. van Veelen ◽  
Tiziana Cervelli ◽  
Mandy W.M.M. van de Rakt ◽  
Arjan F. Theil ◽  
Jeroen Essers ◽  
...  
Keyword(s):  
Dna Damage ◽  
Ionizing Radiation ◽  
Dna Damage Repair ◽  
Damage Repair ◽  
Radiation Induced

RadA: A protein involved in DNA damage repair processes of Deinococcus radiodurans R1

2006 ◽  
Vol 51 (24) ◽  
pp. 2993-2999 ◽  
Author(s):  
Qing Zhou ◽  
Xinjue Zhang ◽  
Hong Xu ◽  
Bujin Xu ◽  
Yuejin Hua
Keyword(s):  
Dna Damage ◽  
Deinococcus Radiodurans ◽  
Dna Damage Repair ◽  
Repair Processes ◽  
Damage Repair ◽  
Deinococcus Radiodurans R1

scholarly journals RecO Is Essential for DNA Damage Repair in Deinococcus radiodurans

2008 ◽  
Vol 190 (7) ◽  
pp. 2624-2628 ◽  
Author(s):  
Guangzhi Xu ◽  
Liangyan Wang ◽  
Huan Chen ◽  
Huiming Lu ◽  
Nanjiao Ying ◽  
...  
Keyword(s):  
Direct Evidence ◽  
Deinococcus Radiodurans ◽  
Uv Light ◽  
Vital Role ◽  
Growth Defect ◽  
Replacement Method ◽  
Damage Repair ◽  
Extreme Sensitivity ◽  
Recf Pathway

ABSTRACT Here we present direct evidence for the vital role of RecO in Deinococcus radiodurans's radioresistance. A recO null mutant was constructed using a deletion replacement method. The mutant exhibited a growth defect and extreme sensitivity to irradiation with gamma rays and UV light. These results suggest that DNA repair in this organism occurs mainly via the RecF pathway.

Absence of DNA damage after 60-Hz electromagnetic field exposure combined with ionizing radiation, hydrogen peroxide, or c-Myc overexpression

2013 ◽  
Vol 53 (1) ◽  
pp. 93-101 ◽  
Author(s):  
Yeung Bae Jin ◽  
Seo-Hyun Choi ◽  
Jae Seon Lee ◽  
Jae-Kyung Kim ◽  
Ju-Woon Lee ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Dna Damage ◽  
Electromagnetic Field ◽  
Ionizing Radiation ◽  
Field Exposure

scholarly journals Lack of the Bacterial Phytochrome Protein Decreases Deinococcus radiodurans Resistance to Mitomycin C

2021 ◽  
Vol 12 ◽  
Author(s):  
Jong-Hyun Jung ◽  
Soyoung Jeong ◽  
Seonghun Im ◽  
Min-Kyu Kim ◽  
Ho Seong Seo ◽  
...  
Keyword(s):  
Dna Damage ◽  
Cell Survival ◽  
Mitomycin C ◽  
Mutant Strain ◽  
Double Mutant ◽  
Deinococcus Radiodurans ◽  
Red Light ◽  
Double Mutant Strain ◽  
Significant Difference

Deinococcus radiodurans known for its extraordinary resistance to ionizing radiation contains bacterial phytochrome (BphP), a member of the family of red/far-red light-sensing proteins. In this study, we constructed a bphP mutant strain (ΔbphP) to investigate the role of D. radiodurans BphP (DrBphP) in the DNA damage response. When cells were incubated under light and dark conditions following exposure to DNA damaging agents, such as γ- and UV-radiation and mitomycin C (MMC), no significant difference in cell survival was observed between the wild-type D. radiodurans strain (WT) and ΔbphP. However, when continuously exposed to MMC under light conditions, the WT strain notably exhibited increased survival compared to cells grown in the dark. The increased survival was not observed in the ΔbphP strain. These results are indicative of the protective role of light-activated DrBphP in the presence of MMC. Site-directed mutagenesis revealed that the conserved amino acids Cys-24 and His-532 involved in chromophore binding and signal transduction, respectively, were essential for the protective function of DrBphP. Inactivation of the cognate response regulator (RR; DrBphR) of DrBphP increased MMC resistance in the dark. In trans complementation of the bphP bphR double mutant strain (ΔbphPR) with DrBphR decreased MMC resistance. Considering that DrBphP acts as a light-activated phosphatase that dephosphorylates DrBphR, it appears that phosphorylated DrBphR exerts a negative effect on cell survival in the presence of MMC. DrBphP overexpression resulted in an increase in MMC resistance of ΔbphPR, implying that other RRs might be involved in the DrBphP-mediated signaling pathway. A mutant lacking the dr_0781 gene (Δdr_0781) demonstrated the same MMC phenotype as ΔbphR. Survival was further increased in the bphR dr_0781 double mutant strain compared to each single mutant ΔbphR or Δdr_0781, suggesting that DR_0781 is also involved in the DrBphP-dependent MMC sensitivity. This study uncovered a previously unknown phenomenon of red/far-red light-dependent DNA damage survival mediated by BphP by identifying the conditions under which DrBphP exhibits a fitness advantage.

scholarly journals The relative biological effectiveness of proton irradiation in dependence of DNA damage repair

2020 ◽  
Vol 93 (1107) ◽  
pp. 20190494 ◽  
Author(s):  
Simon Deycmar ◽  
Erica Faccin ◽  
Tamara Kazimova ◽  
Philip A. Knobel ◽  
Irma Telarovic ◽  
...  
Keyword(s):  
Dna Damage ◽  
Ionizing Radiation ◽  
Treatment Planning ◽  
Radiation Oncology ◽  
Genetic Background ◽  
Proton Irradiation ◽  
Dna Damage Repair ◽  
Personalized Treatment ◽  
Individual Treatment ◽  
Damage Repair

Clinical parameters and empirical evidence are the primary determinants for current treatment planning in radiation oncology. Personalized medicine in radiation oncology is only at the very beginning to take the genetic background of a tumor entity into consideration to define an individual treatment regimen, the total dose or the combination with a specific anticancer agent. Likewise, stratification of patients towards proton radiotherapy is linked to its physical advantageous energy deposition at the tumor site with minimal healthy tissue being co-irradiated distal to the target volume. Hence, the fact that photon and proton irradiation also induce different qualities of DNA damages, which require differential DNA damage repair mechanisms has been completely neglected so far. These subtle differences could be efficiently exploited in a personalized treatment approach and could be integrated into personalized treatment planning. A differential requirement of the two major DNA double-strand break repair pathways, homologous recombination and non-homologous end joining, was recently identified in response to proton and photon irradiation, respectively, and subsequently influence the mode of ionizing radiation-induced cell death and susceptibility of tumor cells with defects in DNA repair machineries to either quality of ionizing radiation. This review focuses on the differential DNA-damage responses and subsequent biological processes induced by photon and proton irradiation in dependence of the genetic background and discusses their impact on the unicellular level and in the tumor microenvironment and their implications for combined treatment modalities.

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