https://orcid.org/0000-0002-4691-3257
Figures & data
Figure 1. Deletion of mazG impairs mycobacterial metabolic adaptation in dormancy model in vitro and during infection of macrophages. Survival of Mtb stains under hypoxic (a) and nutrient-starvation (b) conditions in vitro. The surviving cells were quantified by counting colonies after plating. Compl, complemented mutant strain. Data shown are mean ± SE in triplicate. (c) Cellular NADH/NAD+ ratios in Mtb strains under hypoxic and nutrient-starvation conditions. Thirty-five days after hypoxic/starvation treatment intracellular NADH and NAD+ were extracted and measured as described in Supplementary Materials. Data shown are mean ± SE in duplicate. (d) Functional categories of the differentially expressed genes in the ΔmazG mutant (increase or decrease with fold change >2 vs wt) at 1-day post-infection of THP-1 macrophages. (e) Enrichment analyses of the differentially expressed genes in the ΔmazG mutant according to KEGG pathway. (f) Graphic representation of global metabolic changes in the ΔmazG mutant deduced from enriched pathways according to TubercuList classification and KEGG pathway. Genes showed upregulation and downregulation (ΔmazG vs wt, fold change >2) are indicated in red type and blue type, respectively. FA, fatty acids; 2MC, 2 methylcitrate; 2MIC, 2 methylisocitrate; MM-CoA, methylmalonyl CoA; CIT, citrate; ISOCIT, isocitrate; α-KG, alpha-ketoglutarate; SUC, succinic acid; FUM, fumarate; MAL, malic acid; OAA, oxaloacetate; GLO, glyoxylate; G3P, glycerol 3-phosphate. (g) Graphic illustration of pyrimidine metabolism and its interplay with other metabolic pathways. Metabolic pathways and genes involved in pyrimidine metabolism that showed significantly changed expression in the ΔmazG mutant are indicated in red type and blue type, respectively. Genes required for growth arrest of Mtb under hypoxic condition (Ref. [Citation5]) are underlined. FC, fold change. *p < .05, **p < .01, ***p < .001.
![Figure 1. Deletion of mazG impairs mycobacterial metabolic adaptation in dormancy model in vitro and during infection of macrophages. Survival of Mtb stains under hypoxic (a) and nutrient-starvation (b) conditions in vitro. The surviving cells were quantified by counting colonies after plating. Compl, complemented mutant strain. Data shown are mean ± SE in triplicate. (c) Cellular NADH/NAD+ ratios in Mtb strains under hypoxic and nutrient-starvation conditions. Thirty-five days after hypoxic/starvation treatment intracellular NADH and NAD+ were extracted and measured as described in Supplementary Materials. Data shown are mean ± SE in duplicate. (d) Functional categories of the differentially expressed genes in the ΔmazG mutant (increase or decrease with fold change >2 vs wt) at 1-day post-infection of THP-1 macrophages. (e) Enrichment analyses of the differentially expressed genes in the ΔmazG mutant according to KEGG pathway. (f) Graphic representation of global metabolic changes in the ΔmazG mutant deduced from enriched pathways according to TubercuList classification and KEGG pathway. Genes showed upregulation and downregulation (ΔmazG vs wt, fold change >2) are indicated in red type and blue type, respectively. FA, fatty acids; 2MC, 2 methylcitrate; 2MIC, 2 methylisocitrate; MM-CoA, methylmalonyl CoA; CIT, citrate; ISOCIT, isocitrate; α-KG, alpha-ketoglutarate; SUC, succinic acid; FUM, fumarate; MAL, malic acid; OAA, oxaloacetate; GLO, glyoxylate; G3P, glycerol 3-phosphate. (g) Graphic illustration of pyrimidine metabolism and its interplay with other metabolic pathways. Metabolic pathways and genes involved in pyrimidine metabolism that showed significantly changed expression in the ΔmazG mutant are indicated in red type and blue type, respectively. Genes required for growth arrest of Mtb under hypoxic condition (Ref. [Citation5]) are underlined. FC, fold change. *p < .05, **p < .01, ***p < .001.](/cms/asset/73677606-d998-4ec4-aff0-c7352acec21d/temi_a_1559706_f0001_oc.jpg)
