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Dux promotes metabolism-lactylation-MET cascaded network during early iPSC reprogramming with Brg1 as the histone lactylation reader [RNA-Seq]

ABSTRACT: Dux promotes metabolism-lactylation-MET cascaded network during early iPSC reprogramming with Brg1 as the histone lactylation reader [RNA-Seq]

PROVIDER: PRJNA1055002 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27297269_1.fastq.gz	Fastqsanger.gz
	SRR27297269_2.fastq.gz	Fastqsanger.gz
	SRR27297270_1.fastq.gz	Fastqsanger.gz
	SRR27297270_2.fastq.gz	Fastqsanger.gz
	SRR27297271_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Dux promotes metabolism-lactylation-MET cascaded network during early iPSC reprogramming with Brg1 as the histone lactylation reader

Project description:Dux promotes metabolism-lactylation-MET cascaded network during early iPSC reprogramming with Brg1 as the histone lactylation reader

| PRJNA1054996 | ENA

Dux promotes metabolism-lactylation-MET cascaded network during early iPSC reprogramming with Brg1 as the histone lactylation reader [RNA-Seq]

Project description:The process of reprogramming induced pluripotent stem cells (iPSCs) involves several crucial events, including the shutdown of somatic genes, the mesenchymal-epithelial transition (MET), activation of pluripotent genes, metabolic reprogramming, and epigenetic rewiring. These events intricately interact and influence each other, ultimately leading to the formation of iPSCs. However, the specific element that regulates the reprogramming network remains unclear. Dux, a factor known to promote totipotency during the transition from embryonic stem cells (ESCs) to 2C-like ESCs (2CLC), has not been extensively studied in the context of iPSC reprogramming. In this study, we demonstrate that the modification of H3K18la induced by Dux overexpression controls the metabolism-H3K18la-MET network, enhancing the efficiency of iPSC reprogramming through a metabolic switch and the recruitment of P300 via its C-terminal domain. Through the utilization of H3K18la regulators, we discover that H3K18la plays crucial roles in promoting MET. Furthermore, our proteomic analysis of H3K18la IP experiment uncover the specific recruitment of Brg1 during reprogramming, with both H3K18la and Brg1 being enriched on the promoters of genes associated with epithelial and pluripotency. In summary, our study has demonstrated the significant role of Dux-induced H3K18la in the early reprogramming process, highlighting its function as a potent trigger. Additionally, our research has revealed, for the first time, the binding of Brg1 to H3K18la, indicating its role as a reader of histone lactylation.

2024-03-01 | GSE251640 | GEO

Dux promotes metabolism-lactylation-MET cascaded network during early iPSC reprogramming with Brg1 as the histone lactylation reader [Cut & Tag]

2024-03-01 | GSE251641 | GEO

Dux promotes metabolism-lactylation-MET cascaded network during early iPSC reprogramming with Brg1 as the histone lactylation reader [Cut & Tag]

Project description:Dux promotes metabolism-lactylation-MET cascaded network during early iPSC reprogramming with Brg1 as the histone lactylation reader [Cut & Tag]

| PRJNA1055004 | ENA

Dux promotes OGS-Epigenetic-MET network during early iPSC reprogramming via H3K18la recruiting Brg1

Project description:The process of iPSC reprogramming involves various critical events such as somatic gene shutdown, mesenchymal-epithelial transition (MET), metabolism reprogramming, and epigenetic rewiring. These events interweave and influence each other leading to the formation of the iPSC reprogramming network, thus there appears to be a key element regulating this network. Dux has essential research value by promoting totipotency in the process of transition from ESC to 2C-like ESC and has not been discussed in depth in iPSC reprogramming process. This paper focused on the H3K18la modification linking the OGS-Epigenetic-MET network, which improved the efficiency for iPSC reprogramming via Dux overexpression. Dux promoted H3K18la via metabolism switch, and recruiting P300 through its C-terminal domain, resulting in increasing reprogramming. By using H3K18la regulators, we found the role H3K18la played in promoting MET. We performed proteomic detection of H3K18la by IP combined with MS and found that H3K18la specifically recruited Brg1 in iPSCs. During reprogramming, H3K18la and Brg1 enriched on promoters of epithelial-related genes and pluripotency-related genes. Overall, our work highlights H3K18la as a powerful trigger in the early reprogramming and reveals Dux as a regulator for increasing H3K18la. Brg1 was first demonstrated binding to H3K18la and identified as a reader of lactylation.

2026-02-23 | PXD043547 | Pride

Dux promotes metabolism-lactylation-MET cascaded network during early iPSC reprogramming with Brg1 as the histone lactylation reader

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

2024-03-01 | GSE251642 | GEO

DUX

Project description:DUX

| PRJNA930481 | ENA

A novel dual histone mark reader ZCWPW2 regulates meiotic recombination through lactylation and transcriptional control in humans and mice

Project description:Meiotic recombination ensures proper chromosome segregation and genetic diversity during gametogenesis, and its disruption leads to infertility. It is known that the dual histone methylation writer–reader system, in which PRDM9 deposits H3K4me3 and H3K36me3 marks at nucleosomes to specify recombination hotspots and ZCWPW1 functions as a reader recognizing these marks, is essential for meiotic recombination. However, the regulatory mechanism of this system remains unclear. Here, Deficiency of ZCWPW2 causes recombination defects, with impairment in homologous synapsis and DNA double-strand break repair. CUT&Tag and mass spectrometry analyses revealed that ZCWPW2 recognizes PRDM9-mediated dual histone methylation and interacts with ZCWPW1 to form a complex that recruits recombination-associated proteins to hotspots. Additionally, ZCWPW2 independently binds to promoter regions to regulate meiotic transcription. Lactylome and proteome analyses demonstrated that the ZCWPW1–ZCWPW2 complex interacts with and maintains the activity of lactate dehydrogenase LDHA, and together with ZCWPW2-driven transcription of lactylation writer EP300, to promote lactylation of recombination-associated proteins and stabilize their expression at hotspots. Collectively, we identified ZCWPW2 as a previously unrecognized yet indispensable factor supporting the function of PRDM9/ZCWPW1 during meiotic recombination, elucidated the molecular mechanism of the PRDM9/ZCWPW1/ZCWPW2 system in regulating recombination, and uncovered a critical role for lactylation in meiosis.

2026-01-07 | PXD068838 | Pride

A novel dual histone mark reader ZCWPW2 regulates meiotic recombination through lactylation and transcriptional control in humans and mice

2026-01-07 | PXD070427 | Pride

Assessment of functional overlap between mouse Dux and human DUX4 in vitro and in vivo

Project description:We report both DUX4 and Dux toxicity depend upon their ability to bind DNA and activate transcription. Chromatin immunoprecipitation of V5 epitope tagged human DUX4 and mouse Dux was performed in human myoblasts was analyzed using ChIP-Seq to identify their subsequent binding sites. We found that DUX4 and Dux bind 4-8% of identical sequences, while majority of the binding sites are unique to either DUX4 or Dux. Although small, this overlap could be due to their conserved abilioty to regualte primordial pathways that were essential for life and therefore maintained in both proteins despite their separate evolutionary paths. We performed ChIP-Seq analysis of human myoblasts transfected with plasmids encoding either epitope tagged human DUX4 (1 sample) and mouse Dux (1 sample). Illumina sequencing libraries were prepared from the ChIP and Input DNA, then resulting DNA libraries were quantified and sequenced and aligned to the human genome (hg19).

2015-12-11 | E-GEOD-75791 | biostudies-arrayexpress

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