Fig. 4: Reposition of non-LAD lamina-chromatin binding peaks modulates aging-associated genes in MAD- MSCs. | Nature Communications

Fig. 4: Reposition of non-LAD lamina-chromatin binding peaks modulates aging-associated genes in MAD- MSCs.

From: Disorganized chromatin hierarchy and stem cell aging in a male patient of atypical laminopathy-based progeria mandibuloacral dysplasia type A

Fig. 4

a Distribution of non-LADs lamina-chromatin binding peaks at specific genome loci in WT and MAD-MSCs. Each vertical bar represents one peak out of LADs. b Global non-LAD lamina-chromatin binding peaks identified in WT and MAD-MSCs. The number of the peaks are indicated. c Genome-wide co-occurrence of non-LAD lamina-chromatin binding peaks with promoters using a one-sided permutation test. The vertical axis density represents the frequency of co-occurrence of non-LAD binding peaks with promoters while horizonal axis represents predicted co-occurrence number. The observed co-occurrence number are indicated. d Differentially expressed genes associated with repositioned non-LADs lamina-chromatin binding peaks in MAD-MSCs Genes with over 2-fold transcriptional changes were counted. e Cross-analysis of enrichment of dysregulated genes due to reposition of non-LAD lamina-chromatin binding peaks in MAD-MSCs with geroprotection/senescence-associated profile in different hMSCs aging models. Color depth indicates the enrichment score.

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