To stop evolution: New way of fighting antibiotic resistance demonstrated by Scripps scientists

A team of scientists at The Scripps Research Institute and the University of Wisconsin have demonstrated a new way of fighting antibiotic resistance: by stopping evolution.

In the June issue of the open-access journal PloS Biology, the team describes how a protein called LexA in the bacterium Escherichia coli promotes mutations and helps the pathogen evolve resistance to antibiotics. The scientists also show that E. coli evolution could be halted in its tracks by subjecting the bacteria to compounds that block LexA. Interfering with this protein renders the bacteria unable to evolve resistance to the common antibiotics ciprofloxacin and rifampicin.

"If you inhibit this pathway, the bacteria cannot evolve," says Scripps Research Assistant Professor Floyd Romesberg, Ph.D., who led the study.

Since the evolution of resistance is under the control of LexA, compounds that block the protein might prolong the potency of existing antibiotics.

Evolution -- Its not Like Death and Taxes Anymore

This research raises fundamental questions about evolution. Biologists have often thought about evolution in the same way many think about death and taxes -- something inevitable. But Romesberg is a chemist, and he found himself asking not only how, but why evolution happens.

For the last few years, Romesberg has led an effort to understand the genes that drive evolution, an innovative way of thinking because scientists have more often understood evolution as the force that drives genes. What underlies evolution is mutation -- changes in the DNA. "Mutations are the fuel for evolution," says Romesberg.

Because of the potential harm of mutations, humans and other mammals have evolved to make as few as possible. The machinery inside our cells has the ability to replicate our genomes extremely well, and the "polymerase" enzymes that replicate our DNA rarely make

Contact: Jason Bardi
Scripps Research Institute

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