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GATA‐1‐dependent histone H3K27 acetylation mediates erythroid cell‐specific chromatin interaction between CTCF sites
Author(s) -
Kim Yea Woon,
Kang Yujin,
Kang Jin,
Kim AeRi
Publication year - 2020
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fj.202001526r
Subject(s) - chromatin , ctcf , histone , acetylation , chemistry , microbiology and biotechnology , biology , dna , biochemistry , transcription factor , gene , enhancer
CCCTC‐binding factor (CTCF) sites interact with each other in the chromatin environment, establishing chromatin domains. Our previous study showed that interaction between CTCF sites is cell type‐specific around the β‐globin locus and is dependent on erythroid‐specific activator GATA‐1. To find out molecular mechanisms of the cell type‐specific interaction, we directly inhibited GATA‐1 binding to the β‐globin enhancers by deleting its binding motifs and found that histone H3K27 acetylation (H3K27ac) was decreased at CTCF sites surrounding the β‐globin locus, even though CTCF binding itself was maintained at the sites. Forced H3K27ac by Trichostatin A treatment or CBP/p300 KD affected the interactions between CTCF sites around the β‐globin locus without changes in CTCF binding. Analysis of public ChIA‐PET data revealed that H3K27ac is higher at CTCF sites forming short interactions than long interactions. GATA‐1 was identified as a representative transcription factor that relates with genes present inside the short interactions in erythroid K562 cells. Depletion of GATA‐1‐reduced H3K27ac at CTCF sites near erythroid‐specific enhancers. These results indicate that H3K27ac at CTCF sites is required for cell type‐specific chromatin interactions between them. Tissue‐specific activator GATA‐1 appears to play a role in H3K27ac at CTCF sites in erythroid cells.