AI Article Synopsis
- Antimicrobial resistance (AMR) poses a global threat, and the bacterial SOS response, regulated by LexA and RecA, allows bacteria to gain mutations that contribute to AMR.
- Targeting LexA, which is absent in human cells, with a new inhibitor could suppress the SOS response and thereby lessen the chances of AMR by preventing adaptive mutations.
- Research involving various scientific methods demonstrated that an inhibitor could effectively bind to LexA in Mycobacterium tuberculosis, blocking its function and reducing mutation rates linked to AMR.
Article Abstract
Antimicrobial resistance (AMR) is a serious global threat demanding innovations for effective control of pathogens. The bacterial SOS response, regulated by the master regulators, LexA and RecA, contributes to AMR through advantageous mutations. Targeting the LexA/RecA system with a novel inhibitor could suppress the SOS response and potentially reduce the occurrence of AMR. RecA presents a challenge as a therapeutic target due to its conserved structure and function across species, including humans. Conversely, LexA which is absent in eukaryotes, can be potentially targeted, due to its involvement in SOS response which is majorly responsible for adaptive mutagenesis and AMR. Our studies combining bioinformatic, biochemical, biophysical, molecular, and cell-based assays present a unique inhibitor of mycobacterial LexA, wherein we show that the inhibitor interacts directly with the catalytic site residues of LexA of Mycobacterium tuberculosis (Mtb), consequently hindering its cleavage, suppressing SOS response thereby reducing mutation frequency and AMR.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11408154 | PMC |
| http://dx.doi.org/10.1016/j.jbc.2024.107650 | DOI Listing |
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