GATA-1-dependent histone H3K27ac mediates erythroid cell-specific interaction between CTCF sites
Yea Woon Kim, Yujin Kang, Jin Gu Kang, AeRi Kim
Abstract
Open-access reader
Yea Woon Kim, Yujin Kang, Jin Gu Kang, AeRi Kim
Abstract
Open-access reader
Abstract CTCF sites interact with each other in the chromatin environment, establishing 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 TSA treatment or CBP/p300 KD affected the interactions between CTCF sites around the β-globin locus. Analysis of public ChIA-PET data revealed that H3K27ac is higher at CTCF sites forming short chromatin interactions than long interactions. The short interactions contain erythropoiesis-associated genes and GATA-1 binding sites in erythroid K562 cells. Depletion of GATA-1 reduced H3K27ac at CTCF sites near erythroid enhancers. These results indicate that GATA-1-dependent histone H3K27ac at neighboring CTCF sites mediates erythroid specific chromatin interaction between them.
A significance statement is not available in the OpenAlex record.
A contribution statement is not available in the OpenAlex record.
Method details are not available in the OpenAlex metadata.
Findings are not separately available in the OpenAlex metadata.
Limitations are not available in the OpenAlex metadata.
Application details are not available in the OpenAlex metadata.
Abstract CTCF sites interact with each other in the chromatin environment, establishing 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 TSA treatment or CBP/p300 KD affected the interactions between CTCF sites around the β-globin locus. Analysis of public ChIA-PET data revealed that H3K27ac is higher at CTCF sites forming short chromatin interactions than long interactions. The short interactions contain erythropoiesis-associated genes and GATA-1 binding sites in erythroid K562 cells. Depletion of GATA-1 reduced H3K27ac at CTCF sites near erythroid enhancers. These results indicate that GATA-1-dependent histone H3K27ac at neighboring CTCF sites mediates erythroid specific chromatin interaction between them.
Key concepts: CTCF, Chromatin, Locus control region, Histone, Enhancer, H3K4me3, Hypersensitive site, Biology