CTCF coordinates cell fate specification via orchestrating regulatory hubs with pioneer transcription factors
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ABSTRACT:
PROVIDER: PRJNA978625 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR24799940_1.fastq.gz | Fastqsanger.gz | |||
| SRR24799940_2.fastq.gz | Fastqsanger.gz | |||
| SRR24799941_1.fastq.gz | Fastqsanger.gz | |||
| SRR24799941_2.fastq.gz | Fastqsanger.gz | |||
| SRR24799942_1.fastq.gz | Fastqsanger.gz |
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Project description:CCCTC-binding factor (CTCF), a ubiquitously expressed architectural protein, has emerged as a key regulator of cell identity gene transcription. However, the precise molecular mechanism underlying specialized functions of CTCF remains elusive. Here, we investigate the mechanism through integrative analyses of primary hepatocytes, myocytes, and B cells from mouse and human. We demonstrate that CTCF cooperates with lineage-specific pioneer transcription factors (TFs), including MyoD, FOXA, and PU.1, to control cell identity at 1D and 3D levels. At the 1D level, pioneer TFs facilitate lineage-specific CTCF occupancy via opening chromatin. At the 3D level, CTCF and pioneer TFs form regulatory hubs to govern the expression of cell identity genes. This mechanism is validated using MyoD-null mice, CTCF knockout mice, and CRISPR editing during myogenic differentiation. Collectively, these findings uncover a general mechanism whereby CTCF acts as a cell identity cofactor to control cell identity genes via orchestrating regulatory hubs with pioneer TFs.
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Project description:Pioneer transcription factors critically regulate chromatin organization and hematopoietic cell lineage commitment. During erythropoiesis, hematopoietic stem cells undergo dynamic transcriptional and chromatin remodeling to differentiate into erythrocytes. Functionally validated pioneer factors capable of orchestrating erythropoiesis through dynamic chromatin remodeling remain limited, leaving their regulatory mechanisms incompletely resolved. Here, we identify T-cell acute lymphocytic leukemia 1(TAL1) as a pioneer factor that remodels chromatin to drive transcriptional reprogramming during erythropoiesis. By recruiting SWI/SNF complex, TAL1 drives erythroid fate specification while suppressing alternative lineages through lineage-restricted chromatin compartment reorganization. As a pioneer factor, TAL1 recruits chromatin remodelers BPTF and KMT2A to establish erythroid-specific genomic architecture. These complexes collectively execute TAL1 directed differentiation programs by transcriptionally activating erythroid regulators while repressing non-erythroid determinants. Our work establishes a generalizable chromatin accessibility-directed pioneer factor screening strategy, we identify TAL1 as a master pioneer factor and resolve its mechanism in driving erythroid commitment through 3D epigenome restructuring.
2026-06-24 | GSE305041 | GEO
Project description:Pioneer transcription factors critically regulate chromatin organization and hematopoietic cell lineage commitment. During erythropoiesis, hematopoietic stem cells undergo dynamic transcriptional and chromatin remodeling to differentiate into erythrocytes. Functionally validated pioneer factors capable of orchestrating erythropoiesis through dynamic chromatin remodeling remain limited, leaving their regulatory mechanisms incompletely resolved. Here, we identify T-cell acute lymphocytic leukemia 1(TAL1) as a pioneer factor that remodels chromatin to drive transcriptional reprogramming during erythropoiesis. By recruiting SWI/SNF complex, TAL1 drives erythroid fate specification while suppressing alternative lineages through lineage-restricted chromatin compartment reorganization. As a pioneer factor, TAL1 recruits chromatin remodelers BPTF and KMT2A to establish erythroid-specific genomic architecture. These complexes collectively execute TAL1 directed differentiation programs by transcriptionally activating erythroid regulators while repressing non-erythroid determinants. Our work establishes a generalizable chromatin accessibility-directed pioneer factor screening strategy, we identify TAL1 as a master pioneer factor and resolve its mechanism in driving erythroid commitment through 3D epigenome restructuring.
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Project description:Pioneer transcription factors critically regulate chromatin organization and hematopoietic cell lineage commitment. During erythropoiesis, hematopoietic stem cells undergo dynamic transcriptional and chromatin remodeling to differentiate into erythrocytes. Functionally validated pioneer factors capable of orchestrating erythropoiesis through dynamic chromatin remodeling remain limited, leaving their regulatory mechanisms incompletely resolved. Here, we identify T-cell acute lymphocytic leukemia 1(TAL1) as a pioneer factor that remodels chromatin to drive transcriptional reprogramming during erythropoiesis. By recruiting SWI/SNF complex, TAL1 drives erythroid fate specification while suppressing alternative lineages through lineage-restricted chromatin compartment reorganization. As a pioneer factor, TAL1 recruits chromatin remodelers BPTF and KMT2A to establish erythroid-specific genomic architecture. These complexes collectively execute TAL1 directed differentiation programs by transcriptionally activating erythroid regulators while repressing non-erythroid determinants. Our work establishes a generalizable chromatin accessibility-directed pioneer factor screening strategy, we identify TAL1 as a master pioneer factor and resolve its mechanism in driving erythroid commitment through 3D epigenome restructuring.
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Project description:Pioneer transcription factors critically regulate chromatin organization and hematopoietic cell lineage commitment. During erythropoiesis, hematopoietic stem cells undergo dynamic transcriptional and chromatin remodeling to differentiate into erythrocytes. Functionally validated pioneer factors capable of orchestrating erythropoiesis through dynamic chromatin remodeling remain limited, leaving their regulatory mechanisms incompletely resolved. Here, we identify T-cell acute lymphocytic leukemia 1(TAL1) as a pioneer factor that remodels chromatin to drive transcriptional reprogramming during erythropoiesis. By recruiting SWI/SNF complex, TAL1 drives erythroid fate specification while suppressing alternative lineages through lineage-restricted chromatin compartment reorganization. As a pioneer factor, TAL1 recruits chromatin remodelers BPTF and KMT2A to establish erythroid-specific genomic architecture. These complexes collectively execute TAL1 directed differentiation programs by transcriptionally activating erythroid regulators while repressing non-erythroid determinants. Our work establishes a generalizable chromatin accessibility-directed pioneer factor screening strategy, we identify TAL1 as a master pioneer factor and resolve its mechanism in driving erythroid commitment through 3D epigenome restructuring.
2026-07-06 | GSE337274 | GEO
Project description:Pioneer transcription factors critically regulate chromatin organization and hematopoietic cell lineage commitment. During erythropoiesis, hematopoietic stem cells undergo dynamic transcriptional and chromatin remodeling to differentiate into erythrocytes. Functionally validated pioneer factors capable of orchestrating erythropoiesis through dynamic chromatin remodeling remain limited, leaving their regulatory mechanisms incompletely resolved. Here, we identify T-cell acute lymphocytic leukemia 1(TAL1) as a pioneer factor that remodels chromatin to drive transcriptional reprogramming during erythropoiesis. By recruiting SWI/SNF complex, TAL1 drives erythroid fate specification while suppressing alternative lineages through lineage-restricted chromatin compartment reorganization. As a pioneer factor, TAL1 recruits chromatin remodelers BPTF and KMT2A to establish erythroid-specific genomic architecture. These complexes collectively execute TAL1 directed differentiation programs by transcriptionally activating erythroid regulators while repressing non-erythroid determinants. Our work establishes a generalizable chromatin accessibility-directed pioneer factor screening strategy, we identify TAL1 as a master pioneer factor and resolve its mechanism in driving erythroid commitment through 3D epigenome restructuring.
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Project description:Cell fate commitment is a stepwise process, in which multipotent progenitors transition through sequential regulatory states as they become fate restricted. Recent studies have highlighted the extensive transcriptomic shifts that typify cell differentiation, but our understanding of the epigenetic mechanisms underlying these changes is still superficial. To examine how chromatin states are reorganized during cell fate commitment in an in vivo system, we examined the function of pioneer factor Tfap2a at discrete stages of neural crest development. Our results show that TFAP2a activates distinct sets of genomic regions during induction and specification of neural crest cells. Genomic occupancy analysis revealed that the repertoire of TFAP2a targets depends upon its dimerization with paralogous proteins TFAP2c and TFAP2b. During gastrula stages, TFAP2a/c heterodimers activate components of the neural plate border induction program. As neurulation begins, TFAP2a trades partners, and TFAP2a/b heterodimers reorganize the epigenomic landscape of progenitor cells to promote neural crest specification. We propose that this molecular switch acts to drive progressive cell commitment, remodeling the epigenomic landscape to define the presumptive neural crest. Our findings show how pioneer factors regulate distinct genomic targets in a stage-specific manner, and highlight how paralogy can serve as an evolutionary strategy to diversify the function of the regulators that control embryonic development.
2019-12-12 | GSE126880 | GEO
Project description:Pioneer transcription factors (TFs) regulate cell fate by establishing transcriptionally primed and active states. However, cell fate control requires the coordination of both lineage-specific gene activation and repression of alternative lineage programs, a process that is poorly understood. Here, we demonstrate that the pioneer TF Forkhead box A (FOXA), required for endoderm lineage commitment, coordinates with the PR domain zinc finger 1 (PRDM1) TF to recruit Polycomb repressive complexes, which establish bivalent enhancers and repress alternative lineage programs. Similarly, the pioneer TF OCT4 coordinates with PRDM14 to repress cell differentiation programs in pluripotent stem cells, suggesting this is a common feature of pioneer TFs. We propose that pioneer and PRDM TFs coordinate recruitment of Polycomb complexes to safeguard cell fate.
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