Lamin A/C-promoter interactions specify chromatin state–dependent transcription outcomes

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Figure 5.
Figure 5.

Adipogenic differentiation resets LMNA-promoter interactions. (A) Differentiation of ASCs into adipocytes (21 d; lipids are stained with Oil Red-O). Arrows point to nuclei showing nuclear compaction in adipocytes. Bars, 50 μm. (B) Number of genes interacting with LMNA in ASCs and adipocytes. (C) LMNA peak density map on promoters in adipocytes. (D) Percent of genes that maintain or change expression in adipocytes relative to ASCs, as a function of retention, gain, or loss of LMNA. (Right) Proportions of up- and down-regulated genes that retain, lose, or gain LMNA. (E) Expression heat map for genes with a LMNA-bound promoter in adipocytes (scale, ratio of expressed genes/all genes for a given offset from TSS). (F) Adipogenic promoters lose LMNA association after adipogenic differentiation. Profiles show loss of LMNA from the PPARG P2 promoter and the FABP locus (green arrows), and significant gain of LMNA on the RUNX2 P1 promoter (red arrow). (G) Retention of LMNA on nonadipogenic, lineage-specific promoters (F,G) (log2 ChIP/input ratios).

This Article

  1. Genome Res. 23: 1580-1589

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