Cholesterol metabolism and intrabacterial potassium homeostasis are intrinsically related in <i>Mycobacterium tuberculosis</i>.

ABSTRACT: Potassium (K⁺) is the most abundant intracellular cation, but much remains unknown regarding how K⁺ homeostasis is integrated with other key bacterial biology aspects. Here, we show that K⁺ homeostasis disruption (CeoBC K⁺ uptake system deletion) impedes Mycobacterium tuberculosis (Mtb) response to, and growth in, cholesterol, a critical carbon source during infection, with K⁺ augmenting activity of the Mtb ATPase MceG that is vital for bacterial cholesterol import. Reciprocally, cholesterol directly binds to CeoB, modulating its function, with a residue critical for this interaction identified. Finally, cholesterol binding-deficient CeoB mutant Mtb are attenuated for growth in lipid-rich foamy macrophages and in vivo col

SUBMITTER: Chen Y 

PROVIDER: S-EPMC11601456 | biostudies-literature | 2024 Nov

REPOSITORIES: biostudies-literature