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Lactate regulates major zygotic genome activation by H3K18 lactylation in mammals [RNA-seq]

ABSTRACT: Lactate regulates major zygotic genome activation by H3K18 lactylation in mammals [RNA-seq]

PROVIDER: PRJNA979207 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24821167_1.fastq.gz	Fastqsanger.gz
	SRR24821167_2.fastq.gz	Fastqsanger.gz
	SRR24821168_1.fastq.gz	Fastqsanger.gz
	SRR24821168_2.fastq.gz	Fastqsanger.gz
	SRR24821169_1.fastq.gz	Fastqsanger.gz

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Lactate regulates major zygotic genome activation by H3K18 lactylation in mammals

Project description:Lactate regulates major zygotic genome activation by H3K18 lactylation in mammals

| PRJNA979204 | ENA

Lactate regulates major zygotic genome activation by H3K18 lactylation in mammals [CUT&TAG]

Project description:Lactate regulates major zygotic genome activation by H3K18 lactylation in mammals [CUT&TAG]

| PRJNA979206 | ENA

Lactate regulates major zygotic genome activation by H3K18 lactylation in mammals [CUT&TAG]

Project description:Lactate is present at a high level in the microenvironment of mammalian preimplantation embryos in vivo and in vitro. However, its role in preimplantation development is unclear. Here, we report that lactate is highly enriched in the nuclei of early embryos when major zygotic genome activation (ZGA) occurs in humans and mice. The inhibition of its production and uptake results in developmental arrest at the 2-cell stage, major ZGA failure, and loss of lactate-derived H3K18lac, and the abnormal phenotypes could be recapitulated by overexpression of H3K18R mutation and rescued by addition of Lac-CoA. By profiling the landscape of H3K18lac in human and mouse preimplantation embryos, we show that H3K18lac is enriched on the promoter regions of most major ZGA genes and corelates with their expressions. Taken together, we demonstrate the important role for lactate in major ZGA via H3K18lac, showing a conserved metabolic mechanism underlies preimplantation development of mammalian embryos.

2024-02-14 | GSE234026 | GEO

Lactate regulates major zygotic genome activation by H3K18 lactylation in mammals [RNA-seq]

2024-02-14 | GSE234025 | GEO

Lactate regulates major zygotic genome activation by H3K18 lactylation in mammals.

Project description:Lactate is present at a high level in the microenvironment of mammalian preimplantation embryos in vivo and in vitro. However, its role in preimplantation development is unclear. Here, we report that lactate is highly enriched in the nuclei of early embryos when major zygotic genome activation (ZGA) occurs in humans and mice. The inhibition of its production and uptake results in developmental arrest at the 2-cell stage, major ZGA failure, and loss of lactate-derived H3K18lac, which could be rescued by the addition of Lac-CoA and recapitulated by overexpression of H3K18R mutation. By profiling the landscape of H3K18lac during mouse preimplantation development, we show that H3K18lac is enriched on the promoter regions of most major ZGA genes and correlates with their expressions. In humans, H3K18lac is also enriched in ZGA markers and temporally concomitant with their expressions. Taken together, we profile the landscapes of H3K18lac in mouse and human preimplantation embryos, and demonstrate the important role for H3K18lac in major ZGA, showing that a conserved metabolic mechanism underlies preimplantation development of mammalian embryos.

| S-EPMC10849771 | biostudies-literature

Cancer-Associated Fibroblasts Shape a High-Lactate Microenvironment to Drive Perineural Invasion in Pancreatic Cancer via Histone Lactylation

Project description:Perineural invasion (PNI) is a pivotal prognostic factor in pancreatic cancer, associated with aggressive tumor behavior and adverse patient outcomes. Despite its recognized clinical impact, the molecular mechanisms underlying PNI are not well understood. In this study, we isolated perineural invasion-associated cancer-associated fibroblasts (pCAFs), which demonstrated a markedly enhanced capacity to promote neural invasion in pancreatic cancer compared to non-perineural invasion-associated CAFs (npCAFs). Utilizing single-cell, high-throughput sequencing, and metabolomics, we identified a significant upregulation of glycolysis in pCAFs, fostering a high-lactate tumor microenvironment conducive to cancer progression. pCAFs-derived lactate is absorbed by tumor cells, facilitating histone H3K18 lactylation. This epigenetic modification activates the transcription of neural invasion-associated genes such as L1CAM and SLIT1, thereby driving PNI in pancreatic cancer. Further exploration of metabolic reprogramming in pCAFs revealed enhanced acetylation of the glycolytic enzyme GAPDH, correlated with increased enzymatic activity and glycolytic flux. Targeting of GAPDH and lactylation modifications significantly inhibits neural invasion in a KPC mouse model. Clinical data suggested that high levels of H3K18 lactylation correlate with severe PNI and poorer patient prognosis. Our findings provide critical insights into the role of pCAFs in the PNI of pancreatic cancer, highlighting glycolytic reprogramming and lactate-driven histone modifications as potential therapeutic targets for PDAC.

2025-03-19 | GSE290654 | GEO

Cancer-Associated Fibroblasts Shape a High-Lactate Microenvironment to Drive Perineural Invasion in Pancreatic Cancer via Histone Lactylation [RNA-seq]

2025-03-05 | GSE290845 | GEO

Lactate treatment regulates epigenome of mouse embryonic stem cells (mESCs)

Project description:We treated mESCs with 50mM lactate to examine its impact on mESC epigenome. Interestingly, we found that lactate supplementation stimulated H3K18 lactylation accumulation on a subset of genes, which in turn promoted transcriptional elongation. Our results indicate that lactate supplementation expands transcriptional network of mouse ESCs.

2022-02-01 | GSE192358 | GEO

Lactate regulates major zygotic genome activation by H3K18 lactylation in mammals

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

2024-02-14 | GSE234027 | GEO

Tumor-associated macrophage-derived lactate remodels glioblastoma immune microenvironment through regulation of NHEJ repair by KU70 lactylation

Project description:Glioblastoma (GBM) is a malignancy with a complex tumor microenvironment (TME) dominated by glioblastoma stem cells (GSCs) and infiltrated by tumor-associated macrophages (TAMs), and exhibits aberrant metabolic pathways. Lactate is a critical glycolytic metabolite that promotes tumor progression; however, the mechanisms of lactate transportation and lactylation in the tumor microenvironment (TME) of GBM remain elusive. Here, we found that the lactate metabolic signature was highly expressed in TAMs and tumor cells. Moreover, TAMs provide lactate to GSCs, promoting GSC proliferation and inducing lactylation of the non-homologous end joining (NHEJ) protein KU70 at the residue K317. TAM-derived lactate-mediated KU70 lactylation inhibits cGAS- type I interferon signaling, remodeling the immunosuppressive microenvironment through reduced cytotoxic CD8+ T cell infiltration, promoting the malignant progression of GBM. Combinatorial targeting of lactate transport and immune checkpoints demonstrated additive therapeutic benefit in immunocompetent orthotopic xenograft models. This study unveils TAM-derived lactate and lactylation as a critical regulator of NHEJ and create immunosuppressive microenvironment, linking the TME to DNA damage response in GBM and opening novel avenues for developing combinatorial therapy for GBM.

2024-06-01 | GSE266884 | GEO

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