Extended Data Fig. 9: Effects of lo-siRF-prioritized genes and gene-gene interactions on hypertrophic and non-hypertrophic cell morphology.
From: Epistasis regulates genetic control of cardiac hypertrophy

Relative differences in median cell size (a), normalized peak number (b), and roundness error (c) were analyzed separately for cells size-sorted into the top (hypertrophic cells, green) and bottom (non-hypertrophic cells, orange) microchannel outlets (Extended Data Fig. 7), as well as for all cells combined (blue). For both unaffected (left) and MYH7-R403Q variant (right) cardiomyocytes, the gene-silencing induced relative differences in each morphological feature (a-c) were quantified as \(\left({m}_{s}-{m}_{c}\right)/{m}_{c}\times 100 \%\), where \({m}_{s}\) and \({m}_{c}\) denote median values in gene-silencing and scrambled control conditions, respectively. Squares represent mean relative differences across n = 3 independent cell batches (n = 4 for unaffected cells silencing CCDC141), with overlaid points indicating medians of individual replicates. Violins display mean relative differences from 1,000 bootstrap samples, with error bars indicating standard deviations. Asterisks indicate significant differences compared to scramble controls, based on the maximum p-values of two-sided Mann-Whitney U test across all cell batches (*p < 0.05, **p < 1E-3, ***p < 1E-4). Exact p-values and corresponding cell counts per condition per batch are provided in Source Data.