Spain: Bacteria can now modify their ribosomes in response to antibiotic resistance, according to research published in Nature Communications. The study reveals that Escherichia coli, a bacterium commonly used in research, modifies its ribosomal structures when exposed to the antibiotics streptomycin and kasugamycin. This subtle change reduces the drugs’ ability to target bacterial protein production.
Streptomycin, a key treatment for tuberculosis since the 1940s, and kasugamycin, essential in agriculture for protecting crops from bacterial diseases, both work by interfering with bacterial ribosomes. Ribosomes are complex molecular machines liable for protein synthesis, composed of proteins and ribosomal RNA (rRNA). These structures can be chemically modified to fine-tune protein production in cells.
In response to the antibiotics, researchers discovered that E. coli altered the chemical tags on its ribosomal RNA, particularly in regions where antibiotics typically bind. This modification made it more difficult for the drugs to attach, diminishing their effectiveness. The study highlights an unexpected and subtle survival strategy employed by bacteria to evade drug action.
Anna Delgado-Tejedor, the study’s first author and PhD student at the Center for Genomic Regulation (CRG) in Barcelona stated that, “We believe the bacteria are changing their ribosome system just enough to prevent the antibiotics from binding effectively.”
This discovery adds to the growing list of resistance mechanisms, such as genetic mutations and antibiotic efflux pumps, which bacteria use to survive. However, this novel tactic — modifying ribosomes to avoid antibiotic action — offers a previously unexplored avenue for resistance.
Dr. Eva Novoa, corresponding author of the study, explained that, “It’s a stealthy and precise way for bacteria to dodge drugs.” The research team employed advanced nanopore sequencing technology to observe these chemical modifications directly, a breakthrough that allowed them to study the ribosomes in their natural state without altering the data.
While the study reveals the existence of this mechanism, it does not yet explain why or how the bacteria lose these chemical modifications in response to antibiotics. Future research will explore the biology behind this adaptation and could lead to new strategies to fight antibiotic resistance.
With global antimicrobial resistance claiming over a million lives annually and predicted to cause an additional 39 million deaths by 2050, understanding these new survival strategies is crucial. Dr. Novoa emphasized that, “If we can understand why bacteria shed these modifications, we may develop new drugs or strategies that prevent this and enhance treatment effectiveness.”