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Opposing Role of Dpf2 and Eed on Differentiation of Mouse Embryonic Stem Cells via Regulating Tbx3 (4C)

ABSTRACT: Opposing Role of Dpf2 and Eed on Differentiation of Mouse Embryonic Stem Cells via Regulating Tbx3 (4C)

PROVIDER: PRJEB23413 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR2193445.fastq.gz	Fastqsanger.gz
	ERR2193446.fastq.gz	Fastqsanger.gz
	ERR2193447.fastq.gz	Fastqsanger.gz
	ERR2193448.fastq.gz	Fastqsanger.gz

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Opposing Role of Dpf2 and Eed on Differentiation of Mouse Embryonic Stem Cells via Regulating Tbx3 (4C)

Project description:4C experiments of wild-type and Dpf2 -/- cells to investigate the effect of Dpf2 on the chromatin contacts of Tbx3 locus.

2018-11-30 | E-MTAB-6197 | biostudies-arrayexpress

Opposing Role of Dpf2 and Eed on Differentiation of Mouse Embryonic Stem Cells via Regulating Tbx3 (RNA-seq)

Project description:Opposing Role of Dpf2 and Eed on Differentiation of Mouse Embryonic Stem Cells via Regulating Tbx3 (RNA-seq)

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Opposing Role of Dpf2 and Eed on Differentiation of Mouse Embryonic Stem Cells via Regulating Tbx3 (ChIP-seq)

Project description:ChIP-seq experiments of 3xFlag-Dpf2, Oct4, Sox2 and several histone marks were performed in wild-type and Dpf2 -/- cells to investigate the effect of Dpf2 on the binding of those factors.

2018-11-23 | E-MTAB-6165 | biostudies-arrayexpress

ChIP-Seq to investigate the opposing role of Dpf2 and Eed on differentiation of Mouse Embryonic Stem Cells via regulating Tbx3

Project description:ChIP-Seq to investigate the opposing role of Dpf2 and Eed on differentiation of Mouse Embryonic Stem Cells via regulating Tbx3

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Opposing Role of Dpf2 and Eed on Differentiation of Mouse Embryonic Stem Cells via Regulating Tbx3 (RNA-seq)

Project description:RNA-seq experiments of wild-type E14 cells and Dpf2 knockout cells (OHT treated)

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The BAF and PRC2 Complex Subunits Dpf2 and Eed Antagonistically Converge on Tbx3 to Control ESC Differentiation.

Project description:BAF complexes are composed of different subunits with varying functional and developmental roles, although many subunits have not been examined in depth. Here we show that the Baf45 subunit Dpf2 maintains pluripotency and ESC differentiation potential. Dpf2 co-occupies enhancers with Oct4, Sox2, p300, and the BAF subunit Brg1, and deleting Dpf2 perturbs ESC self-renewal, induces repression of Tbx3, and impairs mesendodermal differentiation without dramatically altering Brg1 localization. Mesendodermal differentiation can be rescued by restoring Tbx3 expression, whose distal enhancer is positively regulated by Dpf2-dependent H3K27ac maintenance and recruitment of pluripotency TFs and Brg1. In contrast, the PRC2 subunit Eed binds an intragenic Tbx3 enhancer to oppose Dpf2-dependent Tbx3 expression and mesendodermal differentiation. The PRC2 subunit Ezh2 likewise opposes Dpf2-dependent differentiation through a distinct mechanism involving Nanog repression. Together, these findings delineate distinct mechanistic roles for specific BAF and PRC2 subunits during ESC differentiation.

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Dpf2 interactome in mouse embryonic stem cells

Project description:Dpf2 is a subunit of the BAF/pBAF chromatin remodelling complex. We have used cross-linking affinity purification-mass spectrometry to explore Dpf2 protein interactions in mouse embryonic stem cells.

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DPF2 reads histone lactylation to drive transcription and tumorigenesis [CUT&TAG]

Project description:Lysine lactylation (Kla) is a new type of histone mark implicated in the regulation of various functional processes such as transcription. However, how this histone mark acts in cancers remains unexplored due in part to a lack of knowledge about its reader proteins. Here, we observe that cervical cancer (CC) cells undergo metabolic reprogram by which lactate accumulation and thereby boost histone lactylation, particularly H3K14la. Utilizing a multivalent photoaffinity probe in combination with quantitative proteomics approach, we identify DPF2 as a candidate target of H3K14la. Biochemical studies as well as CUT&Tag analysis reveal that DPF2 is capable of binding to H3K14la, and co-localizes with it on promoters of oncogenic genes. Notably, disrupting the association between DPF2 and histone lactylation through structure-guided mutation blunts those cancer-related gene expression along with cell survival. Together, our findings reveal DPF2 as a bona fide H3K14la effector that couples histone lactylation to gene transcription and cell survival, offering insight into how histone Kla engages in transcription and tumorigenesis.

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DPF2 reads histone lactylation to drive transcription and tumorigenesis [RNA-seq]

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