Tiny Jumping Genes Fingered as Culprit in Rise of Antibiotic Resistance

criss-crossing DNA strands
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Tiny Jumping Genes Fingered as Culprit in Rise of Antibiotic Resistance

Activity levels of transposons provide the handle needed for selection to spread antibiotic resistance from wild microbes to human pathogens

By Ken Kingery

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 overabundance of “jumping genes,” called transposons, that carry the genetic instructions for resistance from the cell’s source code to plasmids that shuttle between cells.

The results appeared online March 28 in the journal Nature Ecology & Evolution.

“There’s a lot of evidence that suggests human pathogens likely pick up antibiotic resistance from other species living in the natural environment,” said Lingchong You, professor of biomedical engineering at Duke. “Intuitively, it makes sense that high levels of antibiotics in these environments are facilitating the jumping of resistance genes from chromosomes to plasmids so that they can spread, but the underlying mechanism never been directly tested. That’s where our work comes in.”

Read full article on Pratt School of Engineering

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