ArticlePLoS pathogens2023
G9a and Sirtuin6 epigenetically modulate host cholesterol accumulation to facilitate mycobacterial survival.
Article in PLoS pathogens, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Epigenetic modulation in tuberculosis - mycobacterial defense mechanism to host immune responses.Frontiers in immunology · 2026Review
- Inhibition of Histone Methyltransferase G9a Activates Autophagy and Provides Protection in Dry Eye Disease.Investigative ophthalmology & visual science · 2025Article
- Histone demethylase LSD1 regulates lipid homeostasis duringiScience · 2025Article
- Increased autophagy activity regulated by LC3B gene promoter DNA methylation is associated with progression to active pulmonary tuberculosis disease.Respiratory research · 2025Article
- Influence of cell bioenergetics on host-pathogen interaction in the lung.Frontiers in immunology · 2025Review
- Bigger problems from smaller colonies: emergence of antibiotic-tolerant small colony variants of Mycobacterium avium complex in MAC-pulmonary disease patients.Annals of clinical microbiology and antimicrobials · 2024Article
- The impact ofFrontiers in immunology · 2024Review
- Sirtuin-dependent metabolic and epigenetic regulation of macrophages during tuberculosis.Frontiers in immunology · 2023Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cholesterol derived from the host milieu forms a critical factor for mycobacterial pathogenesis. However, the molecular circuitry co-opted by Mycobacterium tuberculosis (Mtb) to accumulate cholesterol in host cells remains obscure. Here, we report that the coordinated action of WNT-responsive histone modifiers G9a (H3K9 methyltransferase) and SIRT6 (H3K9 deacetylase) orchestrate cholesterol build-up in in vitro and in vivo mouse models of Mtb infection. Mechanistically, G9a, along with SREBP2, drives the expression of cholesterol biosynthesis and uptake genes; while SIRT6 along with G9a represses the genes involved in cholesterol efflux. The accumulated cholesterol in Mtb infected macrophages promotes the expression of antioxidant genes leading to reduced oxidative stress, thereby supporting Mtb survival. In corroboration, loss-of-function of G9a in vitro and pharmacological inhibition in vivo; or utilization of BMDMs derived from Sirt6-/- mice or in vivo infection in haplo-insufficient Sirt6-/+ mice; hampered host cholesterol accumulation and restricted Mtb burden. These findings shed light on the novel roles of G9a and SIRT6 during Mtb infection and highlight the previously unknown contribution of host cholesterol in potentiating anti-oxidative responses for aiding Mtb survival.
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Registered trials
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