Scientists unveil the secret behind Superbugs' resistance to antibiotics: the finding that could change everything
Researchers made a “huge breakthrough” when they did an experiment “purely out of curiosity” which solves “a decades-long conundrum” about superbugs.
Antibiotics have been a game changer for humans. Alexander Fleming’s discovery of the first antibiotic, penicillin, in 1928 began a revolution in treating infections saving countless lives. However, bacteria over the past 100 years are now becoming resistant to antibiotics. And these so-called superbugs are a growing problem around the world.
A recent analysis published by the Institute for Health Metrics and Evaluation at the University of Washington estimates that “superbugs could jeopardise food security for over two billion people and increase annual health care costs by US$ 159 billion annually by 2050.” It could also result in the deaths of nearly 40 million people by that time as well.
Fortunately, researchers have made a “huge breakthrough” when they did an experiment “purely out of curiosity” which solves “a decades-long conundrum” about how a critical protein controls genes, switching them on and off, in superbugs. They published the findings this past week in the journal Nature Microbiology.
The secret behind Superbugs' resistance to antibiotics
Bacteria are able to build resistance to antibiotics using a number of defense mechanisms, negating the tools we use to fight off infections in people and animals. One of those involves small DNA molecules in bacterial cells called plasmids, which have their own independent genome, replicate independently and carry antibiotic resistance.
The international study titled “KorB switching from DNA-sliding clamp to repressor mediates long-range gene silencing in a multi-drug resistance plasmid,” initially focused on KorB, a molecule that is essential for the survival of plasmids within their bacterial hosts, using a model plasmid called RK2, a multi-drug resistant plasmid. KorB is known to play a role in controlling gene expression, however, the process wasn’t clear.
Then, fortunately, “a lucky ‘Friday afternoon’ experiment, which was done purely out of curiosity” drew the researchers’ focus to KorA’s ability to lock KorB “in the right place at the right time.” Said postdoctoral researcher at the John Innes Center and first author of the study Dr. Thomas McLean.
The scientists discovered during their research that KorB works in conjunction with molecule KorA by using advanced microscopy and protein crystallography. They found that the two worked together to shut down bacterial gene expression with “KorB acting as a DNA sliding clamp and KorA as a lock which holds KorB in place,” explains the John Innes Center in an article published in Phys.org.
“This was a huge breakthrough that drastically changed the direction of the project,” he added. “Our study provides a new paradigm for bacterial long-range gene regulation and offers a target for novel therapeutics to destabilize plasmids in their host and re-sensitize them to antibiotics.”
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