The culprit behind rising antibiotic resistance -- the overlooked jumping gene

Biomedical engineers at Duke University believe they have discovered the physical mechanism that causes high doses of antibiotics to promote the spread of antibiotic resistance between bacteria

The culprit, they say, is an excess of "jumping genes," or transposons, which carry the genetic instructions for resistance from the cell's source code to the plasmids that shuttle between cells

The findings were published online March 28 in the journal Nature Ecology & Evolution

"There is a lot of evidence that human pathogens may acquire antibiotic resistance from other species living in their natural environment," said Lingchong You, a professor of biomedical engineering at Duke University

The rise of antibiotic resistance in human pathogens is known to coincide with the increase in antibiotic use in large-scale industrial activities such as agriculture and manufacturing

Professor You said that while the cause and effect relationship seemed clear, research had never identified the underlying mechanism

In the newly published paper, You and his postdoc Yao Yi suggest that this mysterious mechanism may be antibiotic-mediated selection for "jumping genes" (called transposons) that switch resistance genes from The chromosomes of the cells are carried to the plasmids

"Yi's experiment was designed to test this possible pathway, which explains how different pathogens acquire resistance from environmental species," You said

Transposons are tiny pieces of DNA that often hop inside cells

In a series of experiments, Yao exposed cells resistant to various antibiotics to a range of concentrations of the antibiotics

"All the curves look almost identical," You said

The number of copies of the transposon on the plasmid affects how much antibiotic-resistant protein a cell makes, the researchers said

However, it was unclear whether higher levels of antibiotics directly caused drug-resistant transposons within these cells to become more active

The levels of antibiotics needed to start driving this selection varied widely between species and specific drugs, the researchers said

"We're now trying to show that this dynamic is actively happening in a real setting, like a hospital, and not just in a petri dish," You said

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