Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genome-wide maps of H3K4me3, H3K9me3 chromatin states in control and Kdm4a knockout oocytes

ABSTRACT: We report the application of low input high-throughput profiling of histone modifications in mouse oocytes. Using antibodies against H3K4me3 (100 oocytes/replicate; 2 biological replicates per genotype) and H3K9me3 ( around 300 oocytes/replicate; 2 biological replicates per genotype), we find that they are mutually exclusive in oocytes and this property is lost in oocytes lacking Kdm4a. H3K9me3 is spread into regions of H3K4me3 postive open chromatin which is surprisingly, well preserved leading to a potential bivalency of scale. Altogether, KDM4A is important to keep H3K4me3 marked open chromatin clear of H3K9me3 spreading in oocytes.

ORGANISM(S): Mus musculus

PROVIDER: GSE129729 | GEO | 2020/01/30

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Genome-wide maps of H3K36me3 in MII oocytes and H3K9me3 in 2-cell embryos

Project description:We report the application of low input high-throughput profiling of histone modifications in mouse oocytes and 2-cell embryos. We used antibodies against H3K36me3 (190 wildtype and 93 knockout MIIcoocytes pooled as one replicate) and H3K9me3 ( around 118 control and MZ embryos / replicate; 1 biological replicates per genotype). In the case of H3K36me3, we find that its establishment and maintence is not affected in oocytes lacking Kdm4a. In the case of H3K9me3 in 2-cell embryos, we find that the histone mark aberrantly gained in Kdm4a deficient oocytes is also maintained in the MZ mutant 2-cell embryo. This shows that Kdm4a is important to keep open chromatin clear of H3K9me3 spreading in oocytes in order to transfer a healthy epigenome amenable for proper genome activation post fertilization.

2020-01-30 | GSE138951 | GEO

2.5 dpc Uterus Chip-Seq of Kdm4a mice

Project description:Purpose: ChipSeq allows us to identify binding sites of target proteins of interest in the genome, helping create a global profile for the same. Kdm4a is a H3K9me3 histone demethylase that acts to prevent spurious accumulation of this repressive mark at H3K4me3 positive transcription start sites. To complement transcriptome data from Kdm4a mice, we performed Chip-Seq on 2.5dpc mouse uterus of 8-10 week old littermate control and Kdm4a knockout mice for Kdm4a, H3K9me3 and H3K4me3. This would help us check which of the target genes with changed gene expression was due to the direct change in histone lanscape in absence of Kdm4a.

2017-08-17 | GSE96591 | GEO

KDM4A regulates the maternal-to-zygotic transition by protecting broad H3K4me3 domains from H3K9me3 invasion in oocytes

Project description:The importance of germline-inherited posttranslational histone modification in priming early mammalian development is just emerging1-4. Histone H3 lysine 9 (H3K9) trimethylation is associated with heterochromatin and gene repression during cell-fate change5, while histone H3 lysine 4 (H3K4) trimethylation marks active gene promoters6. Mature oocytes are transcriptionally quiescent and possess remarkably broad domains of H3K4me3 (bdH3K4me3)1, 2. It remains unknown, which factors contribute to the maintenance of the bdH3K4me3 landscape. Lysine-specific demethylase 4A (KDM4A) demethylates H3K9me3 at promoters marked by H3K4me3 in actively transcribing somatic cells7. Here, we report that KDM4A-mediated H3K9me3 demethylation at bdH3K4me3 in oocytes is crucial for normal preimplantation development and zygotic genome activation (ZGA) after fertilization. Loss of KDM4A in oocytes causes extensive and aberrant H3K9me3 spreading at bdH3K4me3, resulting in insufficient transcriptional activation ZGA genes, endogenous retroviral elements and long terminal repeat -initiated chimeric transcripts in 2-cell embryos. The catalytic activity of KDM4A is essential for normal epigenetic reprogramming and preimplantation development. Hence, KDM4A plays a crucial role in preserving maternal epigenome integrity required for proper ZGA and transfer of developmental control to the embryo.

| EGAS00001004220 | EGA

SMARTSeq_v4 paired end mRNA Seq of Kdm4a control mutant oocytes and preimplantation embryos

Project description:Purpose: The goal of this study was to generate paired-end mRNA Seq transcriptomes of control and Kdm4a mutant oocytes, 2-cell, 4-cell and 8-cell preimplantation embryos to study the dynamics of differentially expressed genes during early development Methods: MII oocytes were isolated from wildtype and Kdm4a knockout mice. 16 MII oocytes from each genotype were washed in M2 medim after zona pellucida removal, washed once in nuclease free water and directly lysed and cDNA prepared according to the manufacturers instructions. Meanwhile, control and knockout MII oocytes were also in vitro fertilised with Kdm4a knockout sperm to produce control (+/-) and maternal mutant (-/-) embryos, and cultured in KSOM EmbryoMax medium (Sigma). 16 embryos were staged each day and harvested according to control embryos. Healthiest mutants were chosen for comparison with minimal secondary effects arising from dead/dying embryos. Similar to oocytes, individual cDNA were prepared and amplified according to manufacturers instructions in nuclease free conditions. Conclusions: Our study represents a detailed analysis of differentially expressed genes in oocytes and embryos lacking maternal and endogenous Kdm4a, with sixteen biological replicates, generated by SMARTSeq v4 paired end RNA-seq technology. The optimized data analysis workflows reported here should provide a framework for comparative investigations of expression profiles between the samples at each developmental stage. Our results show that there is a consistent downrgulation of zygotic genome activation (ZGA) genes in the mutant 2-cell embryos. Mutant 4 and 8-cell embryos have significant upregulation of minor ZGA genes giving us robust statistical significance. We conclude that Kdm4a is required for proper gene activation during maternal-to zygotic transition in conjuction with a permissive chromatin landscape.

2020-01-30 | GSE129731 | GEO

2.5 dpc female HPG axis RNASeq of Kdm4a wildtype and knockout mice

Project description:Purpose: We performed RNA-Seq on 2.5dpc mouse hypothalamus, pituitary, ovary and uterus of 8-10 week old littermate female control and Kdm4a knockout mice. Upon observing for the extent of altered genes of physiological relevance to observed female infertility phenotype, this would help us narrow down the most relevant tissue to perform genome wide ChipSeq binding profiles for Kdm4a, H3K4me3 and H3K9me3. This dataset would present likely target genes under direct control of Kdm4a.

2017-08-17 | GSE96685 | GEO

Genome-wide maps of H3K4me3, H3K9me3 chromatin states in control and Kdm4a knockout oocytes

Project description:Genome-wide maps of H3K4me3, H3K9me3 chromatin states in control and Kdm4a knockout oocytes

| PRJNA532602 | ENA

Efficient Elimination of Acute Myeloid Leukaemia Cells through Inhibition of KDM4A

Project description:We previously identified an essential role for the H3K9me3 histone demethylase, KDM4A, in maintaining AML cell survival, with genetic depletion by shRNA of KDM4A inducing leukaemic cell death with little effect on normal haematopoiesis. We hypothesised KDM4A inhibition may represent a novel and effective strategy to treat AML. To address this, we provided proof-of-principle for the use of KDM4 inhibitors (KDM4Ai) and fully characterised their functional potential in AML cells and identified the epigenetic mechanisms underpinning the essential role of KDM4A activity in THP-1 cells using both ChIP-seq and RNA-seq, delineating and functionally validating the epigenomic network regulated by KDM4A, showing that selective loss of KDM4A is sufficient to induce apoptosis in a broad spectrum of human AML cells. This detrimental phenotype results from a global accumulation of H3K9me3 and H3K27me3 at KDM4A targeted genomic loci thereby causing down-regulation of a KDM4A-PAF1 controlled transcriptional program essential for leukemogenesis, distinct from that of KDM4C.

2022-12-31 | GSE173995 | GEO

Total Stranded paired end RNA Seq of wildtype and knockout Kdm4a 2 cell embryos

Project description:Purpose: The goal of this study was to generate paired-end total RNA Seq transcriptomes of wildtype and Kdm4a 2 cell embryos to study the dynamics of differentially expressed repeats and transposons during early murine development Methods: 2 cell embryos cultured in KSOM EmbryoMax medium (Sigma) were subjected to the SMARTSeq Stranded Total RNASeq protocol according to the manufacturers instructions on the same day simultaneously for control and knockout embryos. Conclusions: Our study represents a detailed analysis of differentially expressed repeats and transposons in embryos lacking maternal or endogenous Kdm4a, with six biologic replicates, generated by SMARTSeq STranded paired end RNA-seq technology. The optimized data analysis workflows reported here should provide a framework for comparative investigations of expression profiles. Our results show that there is a consistent downrgulation of specific LTR families afffected in most biological replicates, by the lack of Kdm4a giving us robust statistical significance. We conclude that Kdm4a is required for proper activation of these repeat elements in conjuction with a permissive chromatin landscape.

2020-01-30 | GSE129733 | GEO

KDM4A regulated genes in human squamous carcinoma cells

Project description:To establish a robust cellular model system for screening genes associated with cell invasion, we over-expressed the oncogenic translocated promoter region (Tpr)-MET proteins in SCC23 cells (SCC23/MET). Using a functional siRNA screen, we identified that the histone demethylase KDM4A played a critical role in the invasive growth and metastasis of SCC mediated by the Oncogenic MET. To investigate the molecular mechanism through which KDM4A inhibit the tumor cell invasion, we knock-down KDM4A in SCC23/MET cell and performed a gene microarray to examine which genes may be regulaged by kDM4A. We generated two stable cell lines. one was infected with virus containing scramble and another infected with virus infected with virus containing KDM4A shRNA. Total RNA were extracted from these two cell lines and subject to microarray.

2013-05-03 | E-GEOD-44238 | biostudies-arrayexpress

KDM4A regulated gene expression in human prostate cancer LNCaP cell

Project description:Histone lysine demethylase KDM4A is overexpressed in prostate cancer and plays a crucial role in tumor growth and survival. To understand the mechanisms underlying KDM4A-depedent cell growth and survival, microarray analysis was performed in LNCaP cells transduced with control or KDM4A specific-knockdown construct. The role of KDM4A in prostate carcinogenesis involves activation of E2F1 and androgen receptor transcriptional profiles. LNCaP cells were transduced by lentivirus carrying control pLKO.1 (empty vector) or shKDM4A construct (KDM4A-specific shRNA) for three days, followed by RNA extraction. Affymetrix GeneChip Human Genome U133 Plus 2.0 Arrays were used for microarray analysis.

2016-07-26 | E-GEOD-77928 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data