DrRRA: a novel response regulator essential for the extreme radioresistance of <i>Deinococcus radiodurans</i>

Wang, Liangyan; Xu, Guangzhi; Chen, Huan; Zhao, Ye; Xu, Nan; Teng, Bing; Hua, Yuejin

doi:10.1111/j.1365-2958.2008.06113.x

Cited by 91 publications

(104 citation statements)

References 39 publications

(44 reference statements)

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“…Our previous studies showed that PprI and RecX participated in the regulation of RecA as positive and negative regulators, respectively, in response to ␥ radiation (19,42). Interestingly a novel protein named Deinococcus radiodurans Response Regulator A (DrRRA) (DR2418) has also been identified for its positive role in the control of RecA expression under stressfree growth conditions, although its expression was constant under radiation stresses regardless of the presence of DrRRA (23). This may suggest that there is a novel regulatory mechanism of RecA in this bacterium.…”

Section: Discussionmentioning

confidence: 99%

Deinococcus radiodurans PprI Switches on DNA Damage Response and Cellular Survival Networks after Radiation Damage

Gao

et al. 2009

Molecular & Cellular Proteomics

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Preliminary findings indicate that PprI is a regulatory protein that stimulates transcription and translation of recA and other DNA repair genes in response to DNA damage in the extremely radioresistant bacterium Deinococcus radiodurans. To define the repertoire of proteins regulated by PprI and investigate the in vivo regulatory mechanism of PprI in response to ␥ radiation, we performed comparative proteomics analyses on wild type (R1) and a pprI knock-out strain ( The Gram-positive nonpathogenic bacterium Deinococcus radiodurans is characterized by extreme resistance to ionizing radiation, UV irradiation, desiccation, and a variety of DNAdamaging agents without resulting in lethality or mutagenesis (1, 2). This dramatic capability is ascribed to its outstanding efficiency in reconstructing a functional genome with high fidelity from hundreds of double strand breaks (DSBs) 1 generated by DNA-damaging agents (2, 3), whereas few other organisms can tolerate DSBs (4). Exponentially growing D. radiodurans is able to withstand 50 -100 times more ionizing radiation than Escherichia coli and can survive a 15-kGy acute ionizing radiation dose with no loss of viability. Its ability of continuous growth without any delay when exposed to a maximum of 60 Gy/h ␥ ray (5) has made it one of the most distinguished candidates for bioremediation of radioactive wastes and contaminants (6, 7). More than 50 years of research has provided many lines of evidence supporting the benefits of the extreme radioresistance of D. radiodurans from its highly efficient DNA damage repair system and its remarkable antioxidation system (1, 8 -15). However, the mechanism underlying its radioresistance is still not completely understood (4, 9). Intriguingly this bacterium not only possesses most of the DNA repair genes found in other organisms but also contains many proteins of yet to be determined functions that have been revealed by genome sequencing and comparative genomics (16,17). These function-unknown proteins may play crucial roles in radioresistance (9, 18) as implied by several studies in this bacterium (19 -23).Several years ago, our group and that of John Battista (19, 22) identified and validated a novel protein, PprI (also named IrrE), essential in D. radiodurans radioresistance. It strongly enhanced catalase activities and promoted the expression of RecA and PprA (19). Expression of the novel gene, driven by the promoter of D. radiodurans groEL (DR0607), also significantly enhanced the resistance of E. coli to ␥ irradiation. We found that the expression of PprI in E. coli also increased the expression of RecA and improved catalase activity (24). Both microarray and Western blotting analysis demonstrated that ionizing radiation did not increase PprI transcription or trans-

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Section: Discussionmentioning

confidence: 99%

Deinococcus radiodurans PprI Switches on DNA Damage Response and Cellular Survival Networks after Radiation Damage

Gao

et al. 2009

Molecular & Cellular Proteomics

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“…8). Superoxide dismutase and catalase activities are decreased and RecA and PprA levels are reduced in the DrRRA gene mutant (645).…”

Section: Continued On Following Pagementioning

confidence: 99%

“…Although recA is strongly induced after irradiation, pprI is constitutively expressed, with no postirradiation induction (368). Under nonstress conditions, the transcriptional regulator DrRRA positively controls the expression of RecA, with no effect under radiation stress (645). The transcriptional regulator DdrO may be responsible for the induction of recA in gamma-irradiated cells (383).…”

Section: Recombinational Processes In D Radiodurans Dna Repairmentioning

confidence: 99%

“…Another novel stress response transcriptional regulator, DrRRA, regulates the expression of numerous genes under normal and ionizing radiation conditions, such as DNA damage-related genes (e.g., recA, pprA, ligT, cinA, gyrB, and uvrB), dps1, genes homologous to plant desiccation resistance proteins, and genes for antioxidant proteins, chaperones, and proteases (645). DrRRA was shown to bind the promoter region of ddrI (DR0997), a DNA damage response gene, the expression of which is significantly reduced in the DrRRA gene mutant under normal and radiation conditions (645). The mutant strain is highly sensitive to ionizing radiation, with a delayed genome reassembly, and moderately sensitive to UV, H 2 O 2 , and desiccation (645) (Fig.…”

Section: Continued On Following Pagementioning

confidence: 99%

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Oxidative Stress Resistance inDeinococcus radiodurans

Slade

Radman

2011

Microbiol Mol Biol Rev

656

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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“…A pool of distinctive genes involved in the stress response has been investigated to explain the extreme resistance of D. radiodurans [17][18][19][20][21][22][23]. Among them, two regulators are noteworthy.…”

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Cooperation of PprI and DrRRA in response to extreme ionizing radiation in Deinococcus radiodurans

Wang

et al. 2012

Chin. Sci. Bull.

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Deinococcus radiodurans possesses extreme resistance to ionizing radiation, and has been engineered for the remediation of toxic components in radioactive environments. We have previously shown that PprI (also named IrrE) and DrRRA are essential for the DNA protection and repair pathways that respond to ionizing radiation stress in this species. Here, we investigated the combined roles of PprI and DrRRA in resistance to gamma radiation (800 Gy). The double mutant, ∆drRRA ∆pprI, was more sensitive to gamma rays than either ∆drRRA or ∆pprI single mutants, and exhibited an elevated level of intracellular protein carbonylation, an extended delay in genome reconstitution and reduced transcriptional levels of certain DNA protection and repair proteins, such as kat, sod, recA and pprA. Interestingly, the induction of DrRRA by ionizing radiation was partially inhibited by the deletion of pprI. Taken together, these results suggest that DrRRA and PprI might have collaborative roles in the response of D. radiodurans to extreme ionizing radiation.

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DrRRA: a novel response regulator essential for the extreme radioresistance of Deinococcus radiodurans

Cited by 91 publications

References 39 publications

Deinococcus radiodurans PprI Switches on DNA Damage Response and Cellular Survival Networks after Radiation Damage

Deinococcus radiodurans PprI Switches on DNA Damage Response and Cellular Survival Networks after Radiation Damage

Oxidative Stress Resistance inDeinococcus radiodurans

Cooperation of PprI and DrRRA in response to extreme ionizing radiation in Deinococcus radiodurans

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