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Integrating transcription factor abundance with chromatin accessibility in human erythroid lineage commitment

ABSTRACT: Integrating transcription factor abundance with chromatin accessibility in human erythroid lineage commitment

PROVIDER: PRJNA705610 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13811411_1.fastq.gz	Fastqsanger.gz
	SRR13811411_2.fastq.gz	Fastqsanger.gz
	SRR13811412_1.fastq.gz	Fastqsanger.gz
	SRR13811412_2.fastq.gz	Fastqsanger.gz
	SRR13811413_1.fastq.gz	Fastqsanger.gz

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Integrating transcription factor abundance with chromatin accessibility in human erythroid lineage commitment

Project description:We present InTAC-seq, a method for simultaneous quantification of genome-wide open chromatin and intracellular protein abundance in fixed cells. Using InTAC we directly observe variation in chromatin accessibility and transcription factor motif occupancy driven by differences in transcription factor protein abundance. By purifying bone marrow progenitor cells based on GATA1 protein expression, we establish its role in both functional and epigenetic restriction of erythroid cell identity in human hematopoiesis.

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Pioneer transcription factor TAL1 reshapes chromatin architecture to direct erythroid cell fate commitment

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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Pioneer transcription factor TAL1 reshapes chromatin architecture to direct erythroid cell fate commitment [CUT&Tag]

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Inferring rules of lineage commitment in haematopoiesis

Project description:Fractionation of EML cells isolated based on surface expression of immunophenotypic markers reveals the existence of a subpopulation that has undergone spontaneous commitment to an erythroid fate. Uncommitted fractions were compared to committed cells, derived from both spontaneous (EryCP) and cytokine-driven (Ediff) commitment. EML cells were separated by flow cytometry based on their expression of the markers Sca1, CD34 and cKit as described.

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