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Other factors must therefore contribute to binding site selectivity. Of note, a motif instance was ?15 times more likely be bound by PPAR�� in L1 adipocytes if it overlapped a region enriched for open chromatin marks in preadipocytes (pFisher Smad signaling influenced by the preadipocyte chromatin state. The majority (79%) of sites bound by PPAR�� in L1s were not shared with hASCs, despite the larger number of sites detected in the latter model. Of note, 34% of L1 PPAR��-binding sites that could not be mapped to the human genome resided within rodent-specific transposable element insertions, which implies that they evolved after the mouse and human lineages diverged. If an L1-binding site could be mapped to an orthologous human sequence, the presence of PPAR�� binding in hASCs correlated with the presence a conserved motif and open chromatin marks (Figure?3C). Evolutionary turnover of DR1-like motifs is therefore likely to contribute to the differential recruitment of PPAR�� and open chromatin marks between the two models. To explore the correlation between PPAR�� recruitment and gene expression, we again assumed that each binding site was associated with the closest known protein-coding gene. We found that genes associated with PPAR�� in L1s check details were approximately three times more likely than nonassociated genes to be upregulated �� 2-fold (pFisher Laccase PPAR��-binding sites that recruit HATs to new locations are more likely to be functionally relevant. Concentrating on genes with ��dynamic�� PPAR��-binding sites that gain H3K27ac in L1s, we found that those for which the orthologous human gene was not associated with H3K27ac in hASCs were significantly more likely to show greater upregulation in L1s than in hASCs and vice versa (pFisher