Surviving the storm: exploring the role of natural transformation in nutrition and DNA repair of stressed Deinococcus radiodurans.

Abstract

Deinococcus radiodurans, a natural transformation (NT)-enabled bacterium renowned for its exceptional radiation resistance, employs unique DNA repair and oxidative stress mitigation mechanisms as a strategic response to DNA damage. This study excavates into the intricate roles of NT machinery in the stressed D. radiodurans, focusing on the genes comEA, comEC, endA, pilT, and dprA, which are instrumental in the uptake and processing of extracellular DNA (eDNA). Our data reveal that NT not only supports the nutritional needs of D. radiodurans under stress but also has roles in DNA repair. The study findings establish that NT-specific proteins (ComEA, ComEC, and endonuclease A [EndA]) may contribute to support the nutritional requirements in unstressed and heavily DNA-damaged cells, while DprA contributes differently and in a context-dependent manner to navigating through the DNA damage storm. Thus, this dual functionality of NT-specific genes is proposed to be a contributing factor in the remarkable ability of D. radiodurans to survive and thrive in environments characterized by high levels of DNA-damaging agents.IMPORTANCEDeinococcus radiodurans is a bacterium known for its extraordinary radiation resistance. This study explores the roles of NT machinery in the radiation-resistant bacterium Deinococcus radiodurans, focusing on the genes comEA, comEC, endA, pilT, and dprA. These genes are crucial for the uptake and processing of eDNA and contribute to the bacterium nutritional needs and DNA repair under stress. The findings suggest that the NT-specific proteins ComEA, ComEC, and EndA may help meet the nutritional needs of unstressed and heavily DNA-damaged cells, whereas DprA plays a distinct role that varies, depending on the context in aiding cells to cope with DNA damage. The functionality of NT genes is proposed to enhance D. radiodurans survival in environments with high levels of DNA-damaging agents.