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. 2019 Oct 15;4(5):e00416-19. doi: 10.1128/mSystems.00416-19

FIG 1.

FIG 1

Properties of L. infantum SNF-resistant mutants. (A) Drug response analysis of wild-type (WT) Leishmania (●) and SNF-resistant mutants LiSNFR50.1 (■), LiSNFR50.2 (♦), LiSNFR50.3 (▲), LiSNFR50.4 (▼), and LiSNFR50.1 grown for 50 passages without SNF (small white box on black background). Data are means ± standard errors of the means (SEM) (error bars) from at least three independent experiments. (B) L. infantum SNF-resistant mutants LiSNFR50.1 (■) and LiSNFR50.3 (▲) have no growth defect compared to wild-type L. infantum (●). Data are means ± SEM from at least three independent experiments. OD600, optical density at 600 nm. (C) Role of AdoMetT1 in SNF resistance. Wild-type L. infantum transfected with empty psp72αHYGα (●) or with LiSNFR50.1 or LiSNFR50.3 transfected with empty psp72αHYGα (■ and ▲, respectively) or with AdoMetT1 cloned into psp72αHYGα (□ and Δ, respectively) were assessed for growth in the presence of increasing concentrations of SNF. Data are means ± SEM for at least three biological replicates. “(H)” in panel C refers to the empty HYG vector.