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In a breakthrough study conducted at Umeå University, Sweden, researchers have uncovered crucial insights into the mechanism behind the spread of antibiotic resistance among bacteria. Published findings reveal how an enzyme plays a pivotal role in dismantling the bacterial cell wall, thereby facilitating the transfer of antibiotic resistance genes.
Associate Professor Ronnie Berntsson, a key author of the study, emphasized the significance of this discovery: “We are adding a piece of the puzzle to the understanding of how antibiotic resistance spreads between bacteria.”
The focus of the research was Enterococcus faecalis, a bacterium notorious for causing difficult-to-treat hospital infections due to its acquired resistance to antibiotics.
The study elucidated that these bacteria utilize Type 4 secretion systems (T4SS) to disseminate resistance traits. T4SS functions akin to a molecular copying device, enabling the transfer of genetic materials, including antibiotic resistance genes, between bacteria.
Central to this process is the enzyme PrgK, which possesses three distinct domains: LytM, SLT, and CHAP. PrgK acts as molecular scissors, cleaving the bacterial cell wall to facilitate the transfer of genetic material.
Surprisingly, the study found that only the SLT domain of PrgK was active, contrary to previous assumptions. The LytM and CHAP domains, although not directly involved in enzymatic activity, play crucial roles in regulating PrgK’s function.
Moreover, researchers identified another T4SS protein, PrgL, which interacts with PrgK to ensure its precise localization within the protein machinery.
Josy ter Beek, a Staff scientist at Umeå University, underscored the implications of these findings: “The insights gained are pivotal for advancing strategies aimed at impeding T4SS-mediated transfer of antibiotic resistance.”
The study employed a multifaceted approach, combining biochemical analyses with functional in vivo studies and structural examinations using advanced techniques such as X-ray crystallography and AlphaFold modelling.
This research marks a significant stride forward in combating the global challenge of antibiotic resistance, offering new avenues for developing targeted interventions to curb its spread among bacterial populations.
