How do E. coli bacteria survive antibiotics according to the IISER Pune study?

E. coli bacteria survive antibiotics by temporarily making extra copies of a key gene, such as folA, which helps them resist drugs like trimethoprim.

What is the role of Lon protease in antibiotic resistance?

The bacterial enzyme Lon protease controls the frequency of gene copy changes, which E. coli uses to adapt and survive antibiotic treatments.

Why is understanding gene copy changes important for fighting antibiotic resistance?

Understanding how gene copy changes help bacteria adapt to antibiotics could lead to better diagnostic tools and treatment strategies to slow down the evolution of drug resistance.

Home / Science / Bacteria's Gene Copy Trick Fuels Superbug Rise

Bacteria's Gene Copy Trick Fuels Superbug Rise

2 Feb

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Summary

E. coli survives antibiotics by making extra copies of a key gene.
Temporary gene duplication aids rapid adaptation to drugs.
Lon protease enzyme controls these gene copy number changes.

Bacteria's Gene Copy Trick Fuels Superbug Rise

Scientists at the Institute of Science Education and Research (IISER), Pune, have discovered a mechanism by which the common bacterium Escherichia coli quickly survives antibiotic treatments. The research, published in eLife and funded by DBT/Wellcome Trust India Alliance, shows that E. coli can temporarily increase its gene copy numbers, specifically for the folA gene, to resist antibiotics like trimethoprim. This gene duplication allows the bacteria to produce more of the targeted protein, enabling survival even when drugs are present.

While these extra gene copies are usually temporary, they provide bacteria with the crucial time needed to develop permanent resistance mutations, potentially explaining the rapid spread of antibiotic resistance globally. The study also identified the bacterial enzyme Lon protease as a controller of these gene copy number fluctuations. Understanding this process could pave the way for improved diagnostic tools and more effective treatment strategies against drug-resistant bacteria.