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Pioneering new enhancers by GATA3: role of facilitating transcription factors and chromatin remodeling

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE280731 | GEO | 2025/06/16

REPOSITORIES: GEO

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Pioneering new enhancers by GATA3: role of facilitating transcription factors and chromatin remodeling [CUTnRUN]

Project description:The mechanistic details by which pioneer transcription factors interact with partner transcription factors and chromatin modification/remodeling enzymes to activate enhancers remains an emerging area of study. Here, we utilize inducible expression of the pioneer factor GATA3 and study cofactor association and structural alterations in local chromatin. ATAC-seq analysis and footprinting revealed co-occurrence of GATA3 with other transcription factors, including AP-1, in newly accessible chromatin. GATA3 and AP-1 co-localize at primed enhancers with p300 and BRG1 where nucleosome positioning is responsive to GATA3 location, not to AP-1. Genetic inhibition of AP-1 binding alters chromatin opening at some, but not most, GATA3-bound loci. Pharmacologic inhibition of SWI/SNF ATPase function results in loss of GATA3-dependent chromatin accessibility, binding, and alterations in local chromatin architecture. We conclude that GATA3-dependent gains in chromatin accessibility require chromatin remodeling and that accessibility at some loci is facilitated by a partner transcription factor, in this case AP-1.

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Pioneering new enhancers by GATA3: role of facilitating transcription factors and chromatin remodeling [RNA-seq]

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Pioneering new enhancers by GATA3: role of facilitating transcription factors and chromatin remodeling [ATAC-seq]

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Pioneering new enhancers by GATA3: role of facilitating transcription factors and chromatin remodeling

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Pioneering new enhancers by GATA3: role of facilitating transcription factors and chromatin remodeling [CUTnRUN]

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Pioneering new enhancers by GATA3: role of facilitating transcription factors and chromatin remodeling [ATAC-seq]

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The chromatin remodeling protein Lsh alters nucleosome occupancy at putative enhancers and modulates binding of lineage specific transcription factors.

Project description:Dynamic regulation of chromatin accessibility is a key feature of cellular differentiation during embryogenesis, but the precise factors that control access to chromatin remain largely unknown. Lsh/HELLS is critical for normal development and mutations of Lsh in human cause the ICF (Immune deficiency, Centromeric instability, Facial anomalies) syndrome, a severe immune disorder with multiple organ deficiencies. We report here that Lsh, previously known to regulate DNA methylation level, has a genome wide chromatin remodeling function. Using micrococcal nuclease (MNase)-seq analysis, we demonstrate that Lsh protects MNase accessibility at transcriptional regulatory regions characterized by DNase I hypersensitivity and certain histone 3 (H3) tail modifications associated with enhancers. Using an auxin-inducible degron system, allowing proteolytical degradation of Lsh, we show that Lsh mediated changes in nucleosome occupancy are independent of DNA methylation level and are characterized by reduced H3 occupancy. While Lsh mediated nucleosome occupancy prevents binding sites for transcription factors in wild type cells, depletion of Lsh leads to an increase in binding of ectopically expressed tissue specific transcription factors to their respective binding sites. Our data suggests that Lsh mediated chromatin remodeling can modulate nucleosome positioning at a subset of putative enhancers contributing to the preservation of cellular identity through regulation of accessibility.

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