Extended Data Fig. 5: Results of GoT analysis are robust to various amplicon UMI thresholds and linear modelling.

a, Frequency of wild-type and mutant cells in HSPCs and MkPs with variable minimum genotyping UMI thresholds (two-sided Fisher’s exact test; see Supplementary Table 6 for sample size). b, Pseudotime comparison between wild-type and mutant cells with an increasing number of thresholds for targeted genotyping UMI (two-sided t-test; see Supplementary Table 6 for sample size). c, Pseudotime comparison between mutant and wild-type cells with UMI threshold of 1 (same datasets as b), with statistical test using a generalized linear model including mutation status and total number of amplicon UMIs per cell. d, Across 100 iterations, the genotyping amplicon UMIs were downsampled to one per cell and the mutant-cell frequency was determined for MkPs or precursor B cells. This frequency was then divided by the total mutant-cell frequency across all progenitor subsets for each of the 100 iterations. Mean ± s.d. after n = 100 downsampling iterations (two-sided Wilcoxon rank-sum test). Essential thrombocythaemia samples with at least 20 cells in each cluster were analysed. e, VAF of CALR mutation in CD34⁺CD38⁻ (left), CD34⁺CD38⁺ (middle) and CD34⁺CD10⁺ (right) FACS-sorted peripheral blood cells from patients with essential thrombocythaemia determined by ddPCR.