Drug-resistant strains of Mycobacterium tuberculosis are difficult to treat and contribute significantly to the global antimicrobial resistance emergency. Here we focus on a potent anti-mycobacterial compound with a new mechanism of action, assumed to inhibit the lysine tRNA synthetase. By isolating and sequencing spontaneous resistant mutants and by analyzing the transcriptional profile of M. tuberculosis treated with different doses of this compound, we aim to better understand its impact on mycobacterial physiology.
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