Additive effects of SbcCD and PolX deficiencies in the in vivo repair of DNA double strand breaks in Deinococcus radiodurans

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

^* To whom correspondence should be addressed. Email: suzanne.sommer{at}igmors.u-psud.fr.

	Abstract

Orthologs of SbcD (Mre11) and SbcC (Rad50) proteins exist in all kingdoms of life and are involved in a wide variety of DNA repair and maintenance functions, including homologous recombination and non homologous 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. 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 possesses a structure-modulated 3'5' exonuclease activity reminiscent of specific nuclease activities displayed by the SbcCD complex from E. coli. We constructed a double mutant devoid of SbcCD and PolX proteins. The double mutant sbcCD polX_Dr 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 excessively numerous, or difficult to repair, DNA lesions.