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. 2017 Oct 31;7:14407. doi: 10.1038/s41598-017-14986-6

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© The Author(s) 2017

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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Large-scale DNA copy-number variation in benznidazole-resistant clones. Histograms showing read-coverage for specific regions of chromosome 11 (a) and 13 (b) in parental and drug-resistant clones. Chromosome annotation was performed by ordering the contigs against the T. cruzi CL Brener reference genome²¹. High read peaks correspond to repetitive hypothetical protein genes, tandem repeats within kinesin-like genes (chromosome 11), linked histone H2A genes and short interspersed DNA sequences (chromosome 13). The red dotted line represents the average read-coverage across all chromosomes (single-copy genes). Assessment by the program control-freeC is consistent with an additional copy (trisomy) of the regions shown in chromosome 11 [from TCRUZ.110005800 (TcCLB.509349.30) to TCRUZ.110020000 (TcCLB.506443.80)] and chromosome 13 [from TCRUZ_130005000 (TcCLB.510165.60) to TCRUZ_130019000 (TcCLB.508325.90)]. Chromosome 11 in clone 2 did not display an increased read-coverage compared to the genome-wide average.