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Identification of PprM: a modulator of the PprI-dependent DNA damage response in Deinococcus radiodurans

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Abstract

Deinococcus radiodurans possesses a DNA damage response mechanism that acts via the PprI protein to induce RecA and PprA proteins, both of which are necessary in conferring extreme radioresistance. In an effort to further delineate the nature of the DNA damage response mechanism in D. radiodurans, we set out to identify novel components of the PprI-dependent signal transduction pathway in response to radiation stress. Here we demonstrate the discovery of a novel regulatory protein, PprM (a modulator of the PprI-dependent DNA damage response), which is a homolog of cold shock protein (Csp). Disruption of the pprM gene rendered D. radiodurans significantly sensitive to γ-rays. PprM regulates the induction of PprA but not that of RecA. PprM belongs in a distinct clade of a subfamily together with Csp homologs from D. geothermalis and Thermus thermophilus. Purified PprM is present as a homodimer under physiological conditions, as the case with Escherichia coli CspD. The pprA pprM double-disruptant strain exhibited higher sensitivity than the pprA or pprM single disruptant strains, suggesting that PprM regulates other hitherto unknown protein(s) important for radioresistance besides PprA. This study strongly suggests that PprM is involved in the radiation response mediated by PprI in D. radiodurans.

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Acknowledgments

We thank Masayuki Iigo and Mitsugu Yamada for valuable comments. This work was supported in part by a Grant-in-Aid for Scientific Research (B) 19380054 from the Japan Society for the Promotion of Science to I. Narumi. H. Sghaier was a Fellow of Advanced Science of the Japan Atomic Energy Agency.

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Correspondence to Issay Narumi.

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Communicated by L. Huang.

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Ohba, H., Satoh, K., Sghaier, H. et al. Identification of PprM: a modulator of the PprI-dependent DNA damage response in Deinococcus radiodurans . Extremophiles 13, 471–479 (2009). https://doi.org/10.1007/s00792-009-0232-8

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  • DOI: https://doi.org/10.1007/s00792-009-0232-8

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