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Pioneer transcription factors coordinate active and repressive gene expression states to regulate cell fate [RNA-seq]

ABSTRACT: Pioneer transcription factors coordinate active and repressive gene expression states to regulate cell fate [RNA-seq]

PROVIDER: PRJNA890270 | ENA |

REPOSITORIES: ENA

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Pioneer transcription factors coordinate active and repressive gene expression states to regulate cell fate [RNA-seq]

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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Pioneer transcription factors coordinate active and repressive gene expression states to regulate cell fate [CUT&Run and ChIP-seq]

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Pioneer transcription factors coordinate active and repressive gene expression states to regulate cell fate

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Pioneer transcription factors coordinate active and repressive gene expression states to regulate cell fate

Project description:This SuperSeries is composed of the SubSeries listed below.

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Pioneer and PRDM transcription factors coordinate bivalent epigenetic states to safeguard cell fate.

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 FOXA coordinates with PRDM1 TF to recruit nucleosome remodeling and deacetylation (NuRD) complexes and Polycomb repressive complexes (PRCs), which establish highly occupied, accessible nucleosome conformation with bivalent epigenetic states, thereby preventing precocious and alternative-lineage gene expression during human endoderm differentiation. Similarly, the pioneer TF OCT4 coordinates with PRDM14 to form bivalent enhancers and repress cell differentiation programs in human pluripotent stem cells, suggesting that this may be a common and critical function of pioneer TFs. We propose that pioneer and PRDM TFs coordinate to safeguard cell fate through epigenetic repression mechanisms.

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Project description:Pioneer transcription factors target compact, transcriptionally silent chromatin, thereby enabling gene activation in development, regeneration, and cell reprogramming. However, silent chromatin is heterogenous, varying in nucleosome mobility, nucleosome compaction, and repressive histone modifications, and how pioneer factors may overcome these different chromatin barriers is unknown. We systematically compared the chromatin targeting of 13 embryonic transcription factors and found that the DNA binding domain (DBD) type predicts whether a pioneer factor targets low-turnover nucleosomes in compact chromatin, dynamic nucleosomes in compact chromatin, or function as non-pioneer factors targeting accessible chromatin. By contrast, non-DBD domains enable targeting of repressed chromatin marked by H3K9me3 or H3K27me3. Fusions of different non-DBD segments of heterochromatin-targeting pioneer factors onto SOX2 can expand binding of Sox2 target motifs, including within heterochromatin, and improve cellular reprogramming. Our study unveils how different forms of silent chromatin are coordinately targeted by lineage-specifying factors.

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