The mechanism of Deinococcus radiodurans pprI gene in enhancing mice radioresistance to r-rays

Objective To investigate the mechanism of Deinococcus radiodurans pprI gene in enhancing mice radioresistance to r-rays by transfecting it in vivo. Methods The male Kunming mice were randomly divided into eontrol group, irradiated group, pCMV-HA transfected group and pCMV-HA-pprl transt~cted group. The pCMV-HA-pprl plasmid contained pprl gene was injected into the muscle of mice which were exposed to total 6 Gy of r-ray irradiation. After injection, the in vivo gene clectroporation technology was used to transfect the pprl gene into the cells, and Western blot was used to identify the Pprl protein, mammalian homolog protein RadSl corresponding to recA gene downstream of pprl, and protein Rad52. Results In the muscle of the mice of transfected pCMV-HA-pprl group, the protein Pprl expressed significantly at 1 d post-irradiation, but there was no expression of pprl gene 7 d post-irradiation and in other groups. In the mice of transfected with pCMV-HA-pprl, the expression of RadS1 protein was significantly increased in the lungs at 1 , 7 and 14 d post-irradiation, and significantly increased in the liver at I and 28 d post-irradiation and increased in the kidneys at 1 and 14 d post-irradition. However, there was no obvious change of Rad52 protein expression in the lungs and livers of mice in all groups. Conlusions The prokaryotic gene pprI could act on the mammalian homologisation analogues radS1 gene downstream of recA gene and then increase the expression level of protein RadS1 which results in the enhancement of radioresistance. Key words: Deinococcus radiodurans;  pprl gene;  in vivo electroporation;  Radiation injury