Deinococcus radiodurans PprI switches on DNA damage response and cellular survival networks after radiation damage

Preliminary findings indicate that Pprl is a regulatory protein that stimulates transcription and translation of recA and other DNA repair genes in response to DNA damage in the extremely radioresistant bacterium Deinococcus radiodurans. To define the repertoire of proteins regulated by Pprl and investigate the in vivo regulatory mechanism of Pprl in response to γ radiation, we performed comparative proteomics analyses on wild type (R1) and a pprl knock-out strain (YR1) tinder conditions of ionizing irradiation. Results of two-dimensional electrophoresis and MALDI-TOF MS or MALDI-TOF/TOF MS indicated that in response to low dose γ ray exposure 31 proteins were significantly up-regulated in the presence of Pprl. Among them, RecA and PprA are well known for their roles in DNA replication and repair. Others are involved in six different pathways, including stress response, energy metabolism, transcriptional regulation, signal transduction, protein turnover, and chaperoning. The last group consists of many proteins with uncharacterized functions. Expression of an additional four proteins, most of which act in metabolic pathways, was down-regulated in irradiated R1. Additionally phosphorylation of two proteins was under the control of Pprl in response to irradiation. The different functional roles of representative Pprl-regulated genes in extreme radioresistance were validated by gene knock-out analysis. These results suggest a role, either directly or indirectly, for Pprl as a general switch to efficiently enhance the DNA repair capability and extreme radioresistance of D. radiodurans via regulation of a series of pathways.