Scientists coaxed the model bacterium Escherichia coli to dramatically resist ionising radiation, a finding that may help understand how organisms can resist radiation damage to cells and repair damaged DNA.
"What our work shows is that the repair systems can adapt and those adaptations contribute a lot to radiation resistance," said University of Wisconsin-Madison Professor Michael Cox, the senior author of the research paper.
In previous work, Cox and his group, working with John R Battista from Louisiana State University, showed that E coli could evolve to resist ionising radiation by exposing cultures of the bacterium to the highly radioactive isotope cobalt-60.
"We blasted the cultures until 99 per cent of the bacteria were dead. Then we'd grow up the survivors and blast them again. We did that twenty times," said Cox.
The result were E coli capable of enduring as much as four orders of magnitude more ionising radiation, making them similar to Deinococcus radiodurans, a desert-dwelling bacterium found in the 1950s to be remarkably resistant to radiation.
That bacterium is capable of surviving more than one thousand times the radiation dose that would kill a human.
"Deinococcus evolved mainly to survive desiccation, not radiation so when conditions are right, it can repair damage very quickly and start growing again," Cox said.
Understanding the molecular machinery that allows some organisms to survive what would otherwise be lethal doses of radiation is important because the same bacterial machinery that repairs DNA and protects cells in microbes exists in humans and other organisms.
Although turning the new findings into application is in the distant future, the results could ultimately contribute designer microbes capable of helping clean radioactive waste sites or making probiotics that could aid patients undergoing radiation therapy for some cancers, researchers said.
The new study demonstrates that organisms can actively repair genetic damage from ionising radiation.
The passive detoxification approach is most likely working in tandem with active mechanisms such as the mutations found by the Wisconsin group as well as other, yet-to-be discovered mechanisms, said Cox.
The study was published in the journal eLife.