Abstract

Deinococcus radiodurans’ extraordinarily strong radiation resistance was attributed to its high Mn²⁺ content. DR1709 was one predicted Mn²⁺ transporter, but after it was disrupted, there were at least ten proteins whose expressions changed markedly, suggesting that the proteins which were expressed differently between the wild type and the mutant may play key roles in this bacterium’s radiation resistance, while DR1709 was only a switch to activate these proteins. To identify if this deduction was true or not, DR1709 was isolated from D. radiodurans and transformed into Escherichia coli BL21, whose genomic background is hugely different from that of D. radiodurans. Results showed that the transformed E. coli had higher resistance to γ and UV radiation than the original strain. After being treated with 150 Gy γ radiation, E. coli containing DR1709 had 70% survival fraction, while only 17% of the control cells can be found on LB plate. DR1709 had the ability to protect cells directly from being damaged by γ and UV radiations. E. coli containingDR1709 had higher Mn content than the initial strain. Although the transformed strain had higher survival than the original E. coli, its survival rate decreased with UV dose increasing. After being transformed with DR1709, E. coli BL21’s Fe content had not changed. DR1709 may be specific for Mn²⁺ and was not responsible for transporting Fe²⁺. Radiation resistance was controlled by multistep in D. radiodurans. Those genes whose expressions were different between the wild type and the DR1709-disrupted mutant were downstream of DR1709. These genes might also play some roles in radiation resistance, but such roles were much less than that played directly by DR1709.

Key words: Deinococcus radiodurans, DR1709, E. coli, Mn, radiation resistance.