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Journal of Bacteriology, July 2007, p. 4784-4790, Vol. 189, No. 13
0021-9193/07/$08.00+0     doi:10.1128/JB.00452-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Additive Effects of SbcCD and PolX Deficiencies in the In Vivo Repair of DNA Double-Strand Breaks in Deinococcus radiodurans{triangledown} ,{dagger}

Esma Bentchikou, Pascale Servant, Geneviève Coste, and Suzanne Sommer*

Université Paris-Sud, CNRS UMR8621, CEA LRC42V, Institut de Génétique et Microbiologie, Bâtiment 409, F-91405 Orsay Cedex, France

Received 27 March 2007/ Accepted 24 April 2007

Orthologs of proteins SbcD (Mre11) and SbcC (Rad50) exist in all kingdoms of life and are involved in a wide variety of DNA repair and maintenance functions, including homologous recombination and nonhomologous end joining. Here, we have inactivated the sbcC and/or sbcD genes of Deinococcus radiodurans, a highly radioresistant bacterium able to mend hundreds of radiation-induced DNA double-strand breaks (DSB). Mutants devoid of the SbcC and/or SbcD proteins displayed reduced survival and presented a delay in kinetics of DSB repair and cell division following {gamma}-irradiation. It has been recently reported that D. radiodurans DNA polymerase X (PolX) possesses a structure-modulated 3'-to-5' exonuclease activity reminiscent of specific nuclease activities displayed by the SbcCD complex from Escherichia coli. We constructed a double mutant devoid of SbcCD and PolX proteins. The double-mutant {Delta}sbcCD {Delta}polXDr (where Dr indicates D. radiodurans) bacteria are much more sensitive to {gamma}-irradiation than the single mutants, suggesting that the deinococcal SbcCD and PolX proteins may play important complementary roles in processing damaged DNA ends. We propose that they are part of a backup repair system acting to rescue cells containing DNA lesions that are excessively numerous or difficult to repair.

* Corresponding author. Mailing address: Institut de Génétique et Microbiologie, Bâtiment 409, Université Paris-Sud, F-91405 Orsay Cedex, France. Phone: 33 (1) 69154614. Fax: 33 (1) 69157808. E-mail: suzanne.sommer{at}igmors.u-psud.fr

{triangledown} Published ahead of print on 4 May 2007.

{dagger} Supplemental material for this article may be found at http://jb.asm.org/.

Journal of Bacteriology, July 2007, p. 4784-4790, Vol. 189, No. 13
0021-9193/07/$08.00+0     doi:10.1128/JB.00452-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Harms, K., Wackernagel, W. (2008). The RecBCD and SbcCD DNases suppress homology-facilitated illegitimate recombination during natural transformation of Acinetobacter baylyi. Microbiology 154: 2437-2445 [Abstract] [Full Text]  
  • Kish, A., DiRuggiero, J. (2008). Rad50 Is Not Essential for the Mre11-Dependent Repair of DNA Double-Strand Breaks in Halobacterium sp. Strain NRC-1. J. Bacteriol. 190: 5210-5216 [Abstract] [Full Text]  
  • Rajpurohit, Y. S., Gopalakrishnan, R., Misra, H. S. (2008). Involvement of a Protein Kinase Activity Inducer in DNA Double Strand Break Repair and Radioresistance of Deinococcus radiodurans. J. Bacteriol. 190: 3948-3954 [Abstract] [Full Text]  


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