DNA binding is essential for PprI function in response to radiation damage in Deinococcus radiodurans

Lu, Haijun; Chen, Huan; Xu, Guangzhi; Shah, Amir Miraj Ul Hussain; Hua, Yuejin

doi:10.1016/j.dnarep.2011.10.013

Cited by 36 publications

(71 citation statements)

References 51 publications

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“…D. radiodurans PprI upregulates 31 proteins and downregulates 4 proteins following 1-kGy irradiation [72]. After 2-kGy irradiation, PprI upregulates the transcription of 210 genes [70]. PprI/DdrO/PprA system seems to be well conserved in genome-sequenced Deinococcus spp., and the divergent orthologs of PprI and DdrO are also found in Meiothermus, Marinithermus, and Oceanithermus spp.…”

Section: Stress Response In D Radioduransmentioning

confidence: 98%

“…Following irradiation, the metalloprotease activity of PprI cleaves DdrO, resulting in induction of the RDR regulon [67 ,69 ]. PprI specifically interacts with the recA and pprA promoters following irradiation [70]. PprI consists of an N-terminal zinc peptidase-like domain, a helix-turn-helix motif, and a C-terminal GAF-like sensory domain.…”

Section: Stress Response In D Radioduransmentioning

confidence: 99%

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DNA repair in hyperthermophilic and hyperradioresistant microorganisms

Ishino

Narumi

2015

Current Opinion in Microbiology

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Section: Stress Response In D Radioduransmentioning

confidence: 98%

Section: Stress Response In D Radioduransmentioning

confidence: 99%

DNA repair in hyperthermophilic and hyperradioresistant microorganisms

Ishino

Narumi

2015

Current Opinion in Microbiology

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“…The recA gene and at least 28 additional genes, many encoding DNA repair proteins, contain a conserved motif called the radiation/desiccation response motif (Makarova et al 2007). Recently, a key regulatory protein, PprI (also called IrrE and DR0167), was shown to bind the recA (and pprA) gene promoters in vitro, and interestingly, was found at the IR-inducible promoters in vivo only after DNA damage (measured by ChIP; Lu et al 2012). PprI itself is constitutively expressed, suggesting that DNA damage leads to posttranslation activation of PprI by some mechanism, but the details are currently unknown.…”

Section: Clpr Regulation In Mycobacteriamentioning

confidence: 99%

DNA Damage Responses in Prokaryotes: Regulating Gene Expression, Modulating Growth Patterns, and Manipulating Replication Forks

Kreuzer

2013

Cold Spring Harbor Perspectives in Biology

208

185

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Recent advances in the area of bacterial DNA damage responses are reviewed here. The SOS pathway is still the major paradigm of bacterial DNA damage response, and recent studies have clarified the mechanisms of SOS induction and key physiological roles of SOS including a very major role in genetic exchange and variation. When considering diverse bacteria, it is clear that SOS is not a uniform pathway with one purpose, but rather a platform that has evolved for differing functions in different bacteria. Relating in part to the SOS response, the field has uncovered multiple apparent cell-cycle checkpoints that assist cell survival after DNA damage and remarkable pathways that induce programmed cell death in bacteria. Bacterial DNA damage responses are also much broader than SOS, and several important examples of LexA-independent regulation will be reviewed. Finally, some recent advances that relate to the replication and repair of damaged DNA will be summarized. Since the publication of DNA Repair and Mutagenesis in 2006 (Friedberg et al. 2006), our understanding of bacterial DNA damage responses has progressed significantly. Some studies have refined known pathways and filled in important details, whereas other studies have uncovered surprising new pathways such as bacterial programmed cell death and a form of replicative repair that reconstitutes severely shattered genomes. This review will focus on these recent advances, with only limited discussion and citation to work that precedes the 2006 tome. THE SOS RESPONSEAs scientists have studied the SOS response in Escherichia coli and other bacteria over the last decade, our understanding of SOS has changed in unexpected ways and the pathway has been found integrated in diverse cellular processes. Our understanding of the mechanism of SOS induction has also advanced in recent years, including a view of induction at the single-cell level. A surprising finding is that the functions of the SOS pathway are not uniform between bacterial species, and so the view of SOS as

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“…PprI was found to speciﬁcally bind the promoters of recA and pprA in vitro but not bind nonspeciﬁc double-strand DNA, suggesting a direct effect of PprI on increasing transcription of these genes. DNA-binding activity is essential for PprI to program the DNA repair process and cellular survival of D.radiodurans in response to radiation damage [23]. …”

Section: Discussionmentioning

confidence: 99%

The effects ofpprIgene ofDeinococcus radioduransR1 on acute radiation injury of mice exposed to 60Co γ-ray radiation

Chen¹,

Wei²,

Zhang³

et al. 2016

Oncotarget

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The role of the pprI gene from Deinococcus radiodurans R1 in therapy of acute radiation injury of a mammalian host was investigated. We injected a plasmid containing the pprI gene into the muscle of mice exposed to total 6Gy of 60Co γ-ray radiation. After injection, we used in vivo gene electroporation technology to transfer the pprI gene into the cell. We found the PprI protein was expressed significantly at 1 d after irradiation, but there was no expression of pprI gene 7 d post-irradiation. The expression of pprI gene evidently decreased the death rate of mice exposed to lethal dose radiation, significantly relieved effects on blood cells in the acute stage, shortened the persistence time of the decrease of lymphocytes, and decreased the apoptotic rates of spleen cells, thymocytes and bone marrow cells. The expression of Rad51 protein in the lungs, livers, and kidneys was significantly higher in the mice treated with the pprI plasmid after irradiation. However, there were no obvious differences for Rad52 protein expression. We conclude that the prokaryotic pprI gene of D. radiodurans R1 first was expressed in mammalian cells. The expressed prokaryotic PprI protein has distinct effects of the prevention and treatment on acute radiation injury of mammal. The effects of radio-resistance may relate to expression of Rad51 protein which is homologous with RecA from D. radiodurans.

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DNA binding is essential for PprI function in response to radiation damage in Deinococcus radiodurans

Cited by 36 publications

References 51 publications

DNA repair in hyperthermophilic and hyperradioresistant microorganisms

DNA repair in hyperthermophilic and hyperradioresistant microorganisms

DNA Damage Responses in Prokaryotes: Regulating Gene Expression, Modulating Growth Patterns, and Manipulating Replication Forks

The effects ofpprIgene ofDeinococcus radioduransR1 on acute radiation injury of mice exposed to 60Co γ-ray radiation

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