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DNA binding is essential for PprI function in response to radiation damage in Deinococcus radiodurans.
DNA Repair (Amst). 2012 Feb 01; 11(2):139-45.DR

Abstract

The extremely radioresistant bacterium Deinococcus radiodurans possesses a rapid and efficient but poorly known DNA damage response mechanism that mobilizes one-third of its genome to survive lethal radiation damage. Deinococcal PprI serves as a general switch to regulate the expression of dozens of proteins from different pathways after radiation, including the DNA repair proteins RecA, PprA and SSB. However, the underlying mechanism is poorly understood. In this study, we analyzed the dynamic alteration in global transcriptional profiles in wildtype and pprI mutant strains by combining microarrays and time-course sampling. We found that PprI up-regulated transcription of at least 210 genes after radiation, including 21 DNA repair and replication-related genes. We purified PprI and a helix-turn-helix (HTH) domain mutant and found that PprI specifically bound to the promoters of recA and pprA in vitro but did not bind nonspecific double-strand DNA. Chromatin immunoprecipitation (ChIP) assays confirmed that PprI specifically interacted with the promoter DNA of recA and pprA after radiation. Finally, we showed that a DNA-binding activity-deficient pprI mutant only partially restored resistance of the pprI mutant strain to γ radiation, UV radiation, and mitomycin C. Taken together, these results indicate that DNA-binding activity is essential for PprI to program the DNA repair process and cellular survival of D. radiodurans in response to radiation damage.

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Publisher Full Text (DOI)

Authors+Show Affiliations

Lu H
Institute of Nuclear-Agricultural Sciences, Key Laboratory of Chinese Ministry of Agriculture for Nuclear-Agricultural Sciences, Zhejiang University, Hangzhou, China.
Chen H
No affiliation info available
Xu G
No affiliation info available
Shah AM
No affiliation info available
Hua Y
No affiliation info available

MeSH

Bacterial ProteinsDNA DamageDNA, BacterialDeinococcusOligonucleotide Array Sequence AnalysisPromoter Regions, GeneticProtein BindingProtein Structure, TertiaryRec A RecombinasesRegulonTranscription, GeneticUp-Regulation

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

22051194

Citation

Lu, Huiming, et al. "DNA Binding Is Essential for PprI Function in Response to Radiation Damage in Deinococcus Radiodurans." DNA Repair, vol. 11, no. 2, 2012, pp. 139-45.
Lu H, Chen H, Xu G, et al. DNA binding is essential for PprI function in response to radiation damage in Deinococcus radiodurans. DNA Repair (Amst). 2012;11(2):139-45.
Lu, H., Chen, H., Xu, G., Shah, A. M., & Hua, Y. (2012). DNA binding is essential for PprI function in response to radiation damage in Deinococcus radiodurans. DNA Repair, 11(2), 139-45. https://doi.org/10.1016/j.dnarep.2011.10.013
Lu H, et al. DNA Binding Is Essential for PprI Function in Response to Radiation Damage in Deinococcus Radiodurans. DNA Repair (Amst). 2012 Feb 1;11(2):139-45. PubMed PMID: 22051194.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - DNA binding is essential for PprI function in response to radiation damage in Deinococcus radiodurans. AU - Lu,Huiming, AU - Chen,Huan, AU - Xu,Guangzhi, AU - Shah,Amir Miraj-Ul-Hussain, AU - Hua,Yuejin, Y1 - 2011/11/02/ PY - 2011/11/5/entrez PY - 2011/11/5/pubmed PY - 2012/5/19/medline SP - 139 EP - 45 JF - DNA repair JO - DNA Repair (Amst) VL - 11 IS - 2 N2 - The extremely radioresistant bacterium Deinococcus radiodurans possesses a rapid and efficient but poorly known DNA damage response mechanism that mobilizes one-third of its genome to survive lethal radiation damage. Deinococcal PprI serves as a general switch to regulate the expression of dozens of proteins from different pathways after radiation, including the DNA repair proteins RecA, PprA and SSB. However, the underlying mechanism is poorly understood. In this study, we analyzed the dynamic alteration in global transcriptional profiles in wildtype and pprI mutant strains by combining microarrays and time-course sampling. We found that PprI up-regulated transcription of at least 210 genes after radiation, including 21 DNA repair and replication-related genes. We purified PprI and a helix-turn-helix (HTH) domain mutant and found that PprI specifically bound to the promoters of recA and pprA in vitro but did not bind nonspecific double-strand DNA. Chromatin immunoprecipitation (ChIP) assays confirmed that PprI specifically interacted with the promoter DNA of recA and pprA after radiation. Finally, we showed that a DNA-binding activity-deficient pprI mutant only partially restored resistance of the pprI mutant strain to γ radiation, UV radiation, and mitomycin C. Taken together, these results indicate that DNA-binding activity is essential for PprI to program the DNA repair process and cellular survival of D. radiodurans in response to radiation damage. SN - 1568-7856 UR - https://www.unboundmedicine.com/medline/citation/22051194/DNA_binding_is_essential_for_PprI_function_in_response_to_radiation_damage_in_Deinococcus_radiodurans_ DB - PRIME DP - Unbound Medicine ER -