However, the entire repair process for DSBs is notably more efficient in DR than in other organisms; DR is able to restore hundreds of copies of damaged double strands in an hour
I guess that answers my last question, but raises another question: what allows the repair process to only be most efficient in DR than other organisms, could there be some other important aspect involved in the mechanism?
The first binding between drRecO and ssDNA occurs in the drSSB-free space of ssDNA and generates a heterotrimer of the drSSB-ssDNA-drRecO complex as an intermediate state. The second binding between drRecO and ssDNA induces the dissociation of drSSB from ssDNA by facilitating a conformational change in ssDNA.
So ultimately from these findings there are two steps involved in a conformational change in the ssDNA and can avoid using ATP?
molecular mechanism of D. radiodurans (DR) RecO (drRecO) in SSB displacement from ssDNA at the single-molecule level. DR is the toughest bacterium known, with outstanding resistance to ionizing radiation and DNA damage-inducing reagents (Blasius et al., 2008; Cox and Battista, 2005; Slade and Radman, 2011), which are the main causes of DSBs, a form of fatal biological damage at the genomic level
I wonder if a section of the genome that helps encode for this mechanism and trait for resistance to ionizing radiation can be inserted in other organisms or be used to prevent DNA damage from radiation