Fig. 7.

The ppsD(G44C) point mutation is responsible for PDIM deficiency and the in vitro growth advantage of the H37Rv PDIM-negative subclone. (A) Thin-layer chromatographic analysis of PDIM biosynthesis. Bacteria were labeled with [¹⁴C]propionate, which is preferentially incorporated into PDIM (6), and cell wall lipids were extracted and separated by thin-layer chromatography. M. tuberculosis H37Rv strains: ppsD+ (lane 1), ppsD(G44C) (lane 2), ppsD rev (lane 3), ppsD(G44C) pMV361-ppsD (lane 4). Results are representative of two independent experiments. (B) Bacteria were grown in 7H9 broth with aeration at 37°C. Growth was monitored by withdrawing aliquots and measuring the OD₆₀₀ at the indicated time points. M. tuberculosis H37Rv strains: ppsD+ (filled squares), ppsD(G44C) (filled circles), ppsD rev (open circles), ppsD(G44C) pMV361-ppsD (open triangles). Results are representative of three independent experiments.