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. 2021 Mar 11;12:1583. doi: 10.1038/s41467-021-21810-3

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© The Author(s) 2021

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. 5 — a Fishplot showing observed fraction of cells with distinct genetic mutations for each sampled timepoint. The co-occurrence of the three mutations in the single-cell data is consistent with a linear model of mutation accumulation. b UMAP embedding of all cells based on measured antibody signal. The cells segregate into six distinct phenotypic clusters with multiple blast compartments. c Average expression of each cell cluster for a selection of markers. d Top row: Same UMAP embedding as in b given as grey outline. For each sampled timepoint, observed cells are plotted and colored according to the detected genotype. Blasts distribute among multiple phenotypic compartments in the final timepoint following FLT3 inhibitor treatment. Middle row: kernel density plot of the CD33 antibody signal resolved by timepoint and genotype. Cells from genotypic compartments with less than ten cells per timepoint are not plotted. Bottom row: bar chart depicting genotypic composition of each phenotypic cluster in b resolved by timepoint. Source data are provided as a Source data file.