
Bacterial ‘jumping genes’ can target and control chromosome ends
On Mar. 6, 2025, Cornell researchers announced they have discovered a new mechanism that genes use to survive and propagate in bacteria with linear DNA, with applications in biotechnology and drug development. Transposons, or “jumping genes” – DNA segments that can move from one part of the genome to another – are key to bacterial evolution and the development of antibiotic resistance.
In a paper published in Science, researchers showed that transposons can target and insert themselves at the ends of linear chromosomes, called telomeres, within their bacterial host. In Streptomyces – historically one of the most significant bacteria for antibiotic development – they found that transposons controlled the telomeres in nearly a third of the chromosomes.
Transposons have been found clustered at the chromosome ends in eukaryotic cells, but this is the first time it’s been documented in bacteria with linear chromosomes, and the researchers found that bacterial transposons (versus eukaryotes) use unique mechanisms to control the telomeres.
Transposons are usually flanked by protein-binding sequences that indicate where to excise the DNA element and move it to a new location. In Streptomyces, researchers observed that the transposons at the telomeres were one-sided, with a traditional transposon sequence on one end with the other end being the telomere. This functionally allows the transposon to be the telomere, making it essential to the cell generally.
The researchers found one subfamily of telomere-targeting transposons that coopted a CRISPR system – normally used by bacteria to defend against viruses – to target and insert itself into the chromosome ends.
The insights – especially into Streptomyces, which is difficult to manipulate in the lab and accounts for the discovery of many of our antibiotics – could prove useful for drug development, as transposons drive bacterial evolution and may direct researchers to new antibiotics and other useful products encoded on these transposons.
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Source: Cornell University
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