Deinococcus radiodurans is a radiation resistant organism with the ability to survive hundreds of DNA double-strand breaks. The compacity to withstand such a detrimental type of DNA break stems from the efficiency of the DNA repair machinery of this organism. D. radiodurans recombination mediator proteins RecO and RecR have been shown to be required for radiation resistance in this organism. In E. coli the RecOR proteins have been reported to stimulate RecA filament nucleation onto SSB-bound single-stranded DNA (ssDNA) through displacement of the SSB protein. However, how D. radiodurans RecO and RecR proteins work to mediate RecA filament formation is not well understand. In this study, we further elucidate the biochemical mechanism of RecOR function; the kinetic evidence demonstrates that D. radiodurans RecOR alter the rate of ATP hydrolysis by the RecA protein when bound to ssDNA regardless of the presence of SSB protein. This effect has not been previously described for other homologous recombination systems. We believe that D. radiodurans RecOR functions to stimulate RecA nucleation to ssDNA directly and independently of SSB protein. Potential mechanisms for this kinetic stimulation will be discussed.
Support or Funding Information
This research was supported by an Institutional Development Award (IDeA) from the National Institute of General Medical Sciences of the National Institutes of Health under grant number R01GM104375 to SLL. RISE, New Mexico-INBRE.
lt;pgt;This research was supported by an Institutional Development Award (IDeA) from the National Institute of General Medical Sciences of the National Institutes of Health under grant number R01GM104375 to SLL. RISE, New Mexico-INBRE. lt;/pgt;
