Journal
CELL
Volume 132, Issue 6, Pages 958-970Publisher
CELL PRESS
DOI: 10.1016/j.cell.2008.01.018
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Funding
- NCI NIH HHS [P50 CA089393-070012, P01 CA080111-090002, P01 CA080111-060002, P50 CA089393, P01 CA8011105, P50 CA089393-060012, P50 CA089393-080012, P01 CA080111, P01 CA080111-010002, P01 CA080111-070002, P01 CA080111-100002, P01 CA080111-080002] Funding Source: Medline
- NHGRI NIH HHS [R01 HG004069-02, 1R01 HG004069-02, R01 HG004069] Funding Source: Medline
- NIDDK NIH HHS [R56 DK074967-01, R56 DK074967, R01DK074967, R01 DK074967, R01 DK074967-01A1] Funding Source: Medline
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Complex organisms require tissue-specific transcriptional programs, yet little is known about how these are established. The transcription factor FoxA1 is thought to contribute to gene regulation through its ability to act as a pioneer factor binding to nucleosomal DNA. Through genome-wide positional analyses, we demonstrate that FoxA1 cell type-specific functions rely primarily on differential recruitment to chromatin predominantly at distant enhancers rather than proximal promoters. This differential recruitment leads to cell type-specific changes in chromatin structure and functional collaboration with lineage-specific transcription factors. Despite the ability of FoxA1 to bind nucleosomes, its differential binding to chromatin sites is dependent on the distribution of histone H3 lysine 4 dimethylation. Together, our results suggest that methylation of histone H3 lysine 4 is part of the epigenetic signature that defines lineage-specific FoxA1 recruitment sites in chromatin. FoxA1 translates this epigenetic signature into changes in chromatin structure thereby establishing lineage-specific transcriptional enhancers and programs.
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