Researchers led by the University of Bath in collaboration with the University of Birmingham observed the evolution of two strains of the soil bacteria Pseudomonas fluorescens (SBW25 and Pf0-1). When the scientists removed a gene that enables the bacteria to swim, both strains of the bacteria quickly evolved the ability to swim again, but using different routes. These findings shed light on how to predict the evolution of bacteria and viruses over time.

The research was published in the journal Nature Communications in a paper titled, “A mutational hotspot that determines highly repeatable evolution can be built and broken by silent genetic changes.”

“Mutational hotspots can determine evolutionary outcomes and make evolution repeatable. Hotspots are products of multiple evolutionary forces including mutation rate heterogeneity, but this variable is often hard to identify,” the researchers wrote. “In this work, we reveal that a near-deterministic genetic hotspot can be built and broken by a handful of silent mutations.”

The researchers compared the DNA sequences of the two strains to understand the differences they observed. They found that in the SBW25 strain, which mutated in a predictable way, there was a region where the DNA strand looped back on itself forming a hairpin-shaped tangle.

“…Our experiments show that we were able to create or remove mutational hotspots in the genome by altering the sequence to cause or prevent the hairpin tangle,” explained Tiffany Taylor, PhD, a research fellow at the Milner Centre for Evolution.”This shows that while natural selection is still the most important factor in evolution, there are other factors at play too.”

“If we knew where the potential mutational hotspots in bacteria or viruses were, it might help us to predict how these microbes could mutate under selective pressure.”

This information can help scientists better understand how bacteria and viruses evolve, which can help in developing vaccines against new variants of diseases. It can also make it easier to predict how microbes might develop resistance to antibiotics.

James Horton, PhD, a postdoc at the Milner Centre for Evolution, added: “Like many exciting discoveries, this was found by accident. The mutations we were looking at were so-called silent because they don’t change the resulting protein sequence, so initially, we didn’t think they were particularly important.

“However our findings fundamentally challenge our understanding of the role that silent mutations play in adaptation.”

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