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. 2019 Dec 9;10:5627. doi: 10.1038/s41467-019-13344-6

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© The Author(s) 2019

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — a Susceptibility to miltefosine (MIL; left panel) and paromomycin (PMM; right panel) were performed on individual clones. The wild-type L. infantum (WT) is shown for both drugs. The MIL resistant mutants were selected after mutagenesis with either EMS or HMPA (Supplementary Table 1) while the PMM-resistant mutants were selected after mutagenesis with EMS, ENU, or MMS (Supplementary Table 1). Data are mean ± SEM. For the MIL susceptibility assay, n = 5 biologically independent replicates for the wild-type and n = 3 biologically independent replicates for the mutants. For the PMM susceptibility assay, n = 3 biologically independent replicates. Statistical analyses were performed using unpaired two-tailed t-tests. ***P < 0.001. b Genome-wide distribution of SNVs in mutants selected against MIL (left panel) and PMM (right panel). Bars represent the genes on each chromosome. Colored bars represent genes mutated in defined numbers of mutant clones; gray bars represent non-mutated genes. Source data are provided as a Source Data file.