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

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 -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 sbcCD polX_Dr (where Dr indicates D. radiodurans) bacteria are much more sensitive to -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.

Published ahead of print on 4 May 2007.

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This article has been cited by other articles:

• 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]