Fig. 7: Viscoelastic substrates regulate genome-wide chromatin accessibility.

a Principal component analysis (PCA) of ATAC-seq data from independent biological replicates of mouse fibroblasts cultured on 2-kPa elastic or viscoelastic (slow relaxing) substrates for 48 h (n = 2 biological replicates). b Percentage of genomic features associated with up- or down-regulated ATAC peaks in viscoelastic groups in comparison with elastic groups. c Heatmap showing the differentially expressed ATAC signals in Ascl1-targeting genomic sites. d ATAC peaks around the promoters of Ascl1 and Myt1l in fibroblasts cultured on elastic and viscoelastic gels. e, f Schematic showing the timeline of Lmna knock-down (e) or HDAC inhibition (f) for reprogramming experiments. g Quantification of the reprogramming efficiency of fibroblasts transfected with negative control or Lmna siRNA and cultured on various surfaces for 7 days (n = 5 independent experiments). h Quantification of the reprogramming efficiency of fibroblasts cultured on various surfaces and in the absence or presence of an HDAC inhibitor (valproic acid, VPA, 2.5 mg ml⁻¹) (n = 5 independent experiments). i Schematic illustrating the effects of viscoelasticity on the cell nucleus. In (g, h), bar graphs show the mean \(\pm\) s.d. and a two-way ANOVA using Tukey’s correction for multiple comparisons was used to determine the significance between the groups. Source data are provided as a Source Data file.