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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 and 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 appears to be clear, research has 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 of "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 say
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
This work was supported by the National Institutes of Health (R01A1125604, R01GM110494, R01EB029466), the National Science Foundation (MCB-1937259), and the David and Lucille Packard Foundation
Journal Reference :
Yi Yao, Rohan Maddamsetti, Andrea Weiss, Yuanchi Ha, Teng Wang, Shangying Wang, Lingchong You.