ArticlePLoS pathogens2025
Cholesterol metabolism and intrabacterial potassium homeostasis are intrinsically related in Mycobacterium tuberculosis.
Article in PLoS pathogens, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Direct bacterial transcript visualization illuminates spatiotemporal environmental adaptation ofScience advances · 2026Article
- Rv3839-Rv3840 links the endogenous heme biosynthesis pathway with Mycobacterium tuberculosis adaptation to nitric oxide and iron limitation stress.PLoS genetics · 2026Article
- The Potassium-Uptake Systems, Trk and Kdp, Coordinately Contribute to Growth Regulation and Survival ofInternational journal of molecular sciences · 2026Article
- Regulatory mechanism of cholesterol transport via LtmA in Mycobacterium smegmatis.Scientific reports · 2026Article
- Rv3839-Rv3840 links the endogenous heme biosynthesis pathway withbioRxiv : the preprint server for biology · 2026Article
- Serine/threonine protein kinase phosphorylation of DosR alters target gene transcription mechanics and regulates Mycobacterium tuberculosis response to nitric oxide stress.PLoS genetics · 2026Article
- CRISPRi-mediated silencing of the ABC transporterFrontiers in microbiology · 2026Article
- Epigenetic modulation in tuberculosis - mycobacterial defense mechanism to host immune responses.Frontiers in immunology · 2026Review
- Novel Multistage SubunitVaccines · 2025Article
- Insights intoFrontiers in cellular and infection microbiology · 2025Article
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3 authors.
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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 colonization. Our findings raise the concept of a role for cholesterol as a key co-factor, beyond its role as a carbon source, and illuminate how changes in intrabacterial K+ levels can act as part of the metabolic adaptation critical for bacterial survival and growth in the host.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.