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. 2024 Mar 9;15:2161. doi: 10.1038/s41467-024-46449-8

Fig. 4. Inactivation of the methionine synthase MetE impacts M. tuberculosis growth in vitro and virulence in vivo under B12 deficient conditions.

Fig. 4

a Expected phenotypes of the M. tuberculosisH37Rv ΔmetE knockout compared to its wild type strain in presence and absence of B12. b and c in vitro growth in liquid (boxed images) and in solid media of the M. tuberculosis H37Rv wild type strain (b) and its ΔmetE mutant (c) in the absence or presence of exogenous B12 and/or L-methionine. d and f Survival rates from SCID mice inoculated by the intranasal route with M. tuberculosis H37Rv and H37Rv ΔmetE fed with normal diet (d) and a B12-deficient diet (f). Each curve represents the pool from 2 independent experiments (n = 12). Statistical analysis was performed using Log-rank (Mantel-Cox) test. e and g Bacterial loads in the lungs of normal (e) and anemic (g) C57BL/6 mice after 24 h, or 4 weeks infected with M. tuberculosis H37Rv and its ΔmetE mutant. Data are mean ± SD of n ≥ 6 biological replicates per mice group. Statistical analysis was performed using unpaired t-test. p values are as follows: ****0.0001 > p; ***0.001 > p > 0.0001; p ≥ 0.05; ns: not significant. Results show that inactivation of the methionine synthase MetE attenuates the M. tuberculosis virulence more markedly in B12 anemic mice relative to controls.