Bacteria change their ribosomes when they come into contact with common antibiotics, recent findings show. These modified ribosomes have alterations in the areas where antibiotics attach and disrupt protein synthesis. The research highlights these changes enhance bacterial resistance to the medications. This subtle transformation may alter the binding sites of the drugs, presenting a potential new way that bacteria resist antibiotics.
Bacteria change their ribosomes when exposed to common antibiotics, as indicated by a study released today in Nature Communications. These subtle transformations may influence the drug-binding sites, indicating a possible new mechanism of antibiotic resistance.
Escherichia coli, a frequently harmless bacterium, can lead to severe infections. The study involved exposing E. coli to streptomycin and kasugamycin, two antibiotics used to treat bacterial infections. Streptomycin has been used since the 1940s to manage tuberculosis and various infections, while kasugamycin, though less commonly recognized, plays a vital role in agriculture to safeguard crops against bacterial diseases.
Both antibiotics disrupt the bacteria’s capacity to produce new proteins by targeting their ribosomes. These ribosomes are vital molecular structures composed of proteins and ribosomal RNA, which often undergo chemical modifications that can change the ribosome’s shape and function. These chemical tags assist cells in regulating protein synthesis efficiently.
The research revealed that E. coli starts forming new ribosomes that differ slightly from those generated under normal conditions when exposed to these antibiotics. Depending on the antibiotic, the new ribosomes were found to lack specific chemical tags, especially in the regions where the drugs bind to impede protein synthesis. This modification helps the bacteria become more resistant to these antibiotics.
“It seems that the bacteria’s ribosomes are changing their structure just enough to hinder effective binding of the antibiotic,” comments Anna Delgado-Tejedor, the study’s lead author and a PhD student at the Centre for Genomic Regulation (CRG) in Barcelona.
Bacteria have various strategies for developing antibiotic resistance, including mutations in their DNA. They may also actively expel antibiotics out of their cells, reducing concentrations to non-harmful levels.
This research reveals a new survival strategy. “E. coli is modifying its molecular structures with impressive precision and in real time. It’s a clever and subtle method to evade drug effects,” remarks Dr. Eva Novoa, the study’s corresponding author and a researcher at CRG.
The findings were achieved using advanced nanopore sequencing technology, which directly analyzes RNA molecules. Previous methods often removed chemical modifications during processing. “Our method has enabled us to observe the modifications in their natural context,” explains Dr. Novoa.
The study does not delve into the reasons behind the loss of these chemical modifications. Future research could investigate the biological mechanisms behind this adaptability and potentially reveal new methods to address one of the most pressing global health challenges. Since 1990, antimicrobial resistance has resulted in at least one million deaths annually and is projected to cause an additional 39 million fatalities by 2050.
“By gaining a deeper understanding of why these modifications are diminished, we can develop strategies to prevent this shedding or design new drugs that more effectively bind to the modified ribosomes,” adds Dr. Novoa.
