Researchers have discovered a previously unknown mechanism that allows bacteria to develop antibiotic resistance far faster than scientists thought possible, a finding that could point toward new ways to slow it down.
For the study, published in Nature Microbiology, researchers at Technion built a new computational tool called AmpliFinder to scan more than 10,000 laboratory-evolved bacterial samples for patterns of gene duplication.
Gene amplification is a well-known evolutionary trick. But the researchers uncovered a dramatic, previously overlooked version of it: a “non-canonical” form in which genes are duplicated through a single DNA segment linking distant regions of the genome, making the process much harder to detect using standard methods. Using AmpliFinder, the team found that these non-canonical amplifications aren't rare exception —they're common, and efficient at churning out gene copies.
Working with two common bacterial species, Escherichia coli and Acinetobacter baumannii, the researchers treated the microbes with the antibiotic chloramphenicol and observed amplification of a DNA segment carrying the mdfA gene. That amplification not only strengthened the bacteria's existing resistance but let them adapt to progressively higher antibiotic concentrations—evidence that this mechanism drives significantly faster evolution than previously recognized pathways.
"When we began our research, we expected to identify mainly the classical amplification mechanism described in textbooks, a repetitive structure of a gene flanked by two copies of the same mobile genetic element," said study author Idan Yelin, professor of biology at Technion. "We assumed that the non-canonical structures would be little more than a footnote. Instead, that footnote turned out to be the main story.”
The findings suggest this hidden pathway may be a major driver of the antibiotic resistance crisis, which has accelerated alongside decades of antibiotic overuse. The researchers say identifying the mechanism opens the door to therapies designed specifically to disrupt it, potentially blunting bacteria's ability to adapt and helping existing antibiotics stay effective for longer.
Data from Technion-Israel Institute of Technology