The gene is responsible for intrinsic resistance to various drugs and virulence in by regulating cell division.

exhibits intrinsic resistance to most antibiotics, hence leading to infections that are difficult to treat. To address this issue, the identification of new molecular targets is essential for the development or repositioning of therapeutic agents. This study demonstrated that the -knockout strain, Mab, became significantly susceptible to a range of antibiotics, not only but also exhibited susceptibility to rifabutin, bedaquiline, and linezolid . While the bacterial burden of the wild-type (Mab) increased by over 1 log CFU/lung in a murine infection model 16 days post-infection, that of Mab strain decreased by more than 1 log CFU/lung, which suggests that the disruption leads to attenuation. Bioinformatics analysis revealed that MAB_2362 shares the highest similarity (41.35%) with SteA, a protein known to influence cell division in , suggesting that MAB_2362 might be involved in cell division. Mab cells exhibited a median length of 2.62 µm, which was substantially longer than the 1.44 µm recorded for Mab cells. Additionally, multiple cell division septa were observed in 42% of Mab cells, whereas none were seen in Mab cells. An ethidium bromide uptake assay further suggested a higher cell envelope permeability in Mab compared to Mab. Collectively, these findings underscore the role of in intrinsic resistance and virulence of possibly through the regulation of cell division. Thus, MAB_2362 emerges as a promising candidate for targeted interventions in the pursuit of novel antimicrobials against .