Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Characterization and function of transcriptional elongation during zygotic genome activation in mouse embryos [ChIP-seq]

ABSTRACT: Characterization and function of transcriptional elongation during zygotic genome activation in mouse embryos [ChIP-seq]

PROVIDER: PRJNA802238 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR17838412_1.fastq.gz	Fastqsanger.gz
	SRR17838412_2.fastq.gz	Fastqsanger.gz
	SRR17838413_1.fastq.gz	Fastqsanger.gz
	SRR17838413_2.fastq.gz	Fastqsanger.gz
	SRR17838414_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 36

Similar Datasets

Characterization and function of transcriptional elongation during zygotic genome activation in mouse embryos [RNA-seq]

Project description:The work associated to these datasets focuses on the investigation of transcriptional regulation during the earliest stages of mammalian embryogenesis. In particular, ChILseq and RNAseq datasets were generated to study the process of zygotic genome activation in mouse embryos. After fertilisation, the mouse embryo activates its own genome for the first time in a process known as zygotic genome activation, which occurs primarily on two main waves. The first wave occurs in zygotes, and the second one at the late 2-cell stage. To understand how the RNA Polymerase II functions during these waves, we have implemented a ChILseq approach to generate genome-wide maps of Ser5 and Ser2 phosphorylated forms of RNA Polymerase II in zygotes, 2- and 8-cell stage embryos. In addition, we have investigated how elongation factors, such as NELF and DSIF regulate major ZGA by performing single embryo RNAseq using SMART-seq2 in 2-cell stage embryos upon depletion of Spt5, NELFE and upon chemical inhibition of Cdk9.

2022-10-01 | GSE195839 | GEO

Characterization and function of transcriptional elongation during zygotic genome activation in mouse embryos [ChIP-seq]

2022-10-01 | GSE195830 | GEO

Characterization and function of transcriptional elongation during zygotic genome activation in mouse embryos [ChIL-seq]

2022-10-01 | GSE195827 | GEO

Characterization and function of transcriptional elongation during zygotic genome activation in mouse embryos

Project description:Characterization and function of transcriptional elongation during zygotic genome activation in mouse embryos

| PRJNA802259 | ENA

Characterization and function of transcriptional elongation during zygotic genome activation in mouse embryos [RNA-seq]

Project description:Characterization and function of transcriptional elongation during zygotic genome activation in mouse embryos [RNA-seq]

| PRJNA802262 | ENA

Characterization and function of transcriptional elongation during zygotic genome activation in mouse embryos [ChIL-seq]

Project description:Characterization and function of transcriptional elongation during zygotic genome activation in mouse embryos [ChIL-seq]

| PRJNA802235 | ENA

Characterization of Zygotic Genome Activation-dependent Maternal mRNA Clearance in Mammals

Project description:A conserved event of the maternal-to-zygotic transition (MZT) in animal embryos is the elimination of a subset of the maternal transcripts that accumulated during oogenesis. In invertebrates and lower vertebrates, a maternally encoded mRNA decay pathway (M-decay) acts before zygotic genome activation (ZGA) while a second pathway, which requires zygotic transcription, subsequently clears additional mRNAs (Z-decay). To date it has not been clear whether a Z-decay pathway is present in mammals. Here, we identify mouse and human maternal transcripts that are degraded after ZGA and show that inhibition of de novo transcription stabilizes these mRNAs in mouse and human embryos. We show that YAP1-TEAD4 transcription factor-mediated transcription is essential for Z-decay in mouse embryos and that TEAD4-triggered zygotic Tut4/7 expression and mRNA 3ʹ-oligouridylation direct Z-decay.

2019-11-12 | GSE128283 | GEO

Quantitative proteomics reveals the dynamic proteome landscape of zebrafish embryos during maternal-to-zygotic transition and its relationship to zygotic genome activation

Project description:Upon fertilization, the embryonic genome remains transcriptionally inactive until the mid-blastula transition. Zygotic genome activation (ZGA) of vertebrate embryos has been extensively studied using nucleic acid-based strategies, but proteomics data are still scarce, impeding the full mechanistic understanding of how ZGA is executed during the maternal-to-zygotic transition (MZT). Here, we performed quantitative proteomics to decipher the proteome landscape of zebrafish embryos during the MZT, quantifying nearly 5,000 proteins across four embryonic stages. The stage-specific clustering based on protein expression pattern revealed that helicases (i.e., eif4a2 and ruvbl1) facilitate pluripotency factors (i.e., nanog, pou5f3, ctcf, and hmga1) triggering ZGA in zebrafish, accompanied by the maternal product decay with P-bodies and ubiquitin dependent proteolytic pathway. Dozens of transcription factors show wave-like expression patterns during MZT, implying their diverse functions in triggering the ZGA and modulating differentiation for organ development. The combination of morpholino knockdown and quantitative proteomics demonstrated that maternal Nanog is required for proper embryogenesis by regulating 1) interactions with other pluripotency factors, 2) F-actin band formation, 3) cell cycle checkpoints and 4) maternal product degradation. This study represents the most systematic proteomics survey of developmentally regulated proteins and their expression profiles accompanying MZT in zebrafish, which is a valuable proteome resource for understanding ZGA.

2024-05-01 | PXD036678 | Pride

Unreprogrammed H3K9me3 prevents minor zygotic genome activation and lineage commitment in SCNT embryos

Project description:Somatic cell nuclear transfer (SCNT) can be used to reprogram differentiated somatic cells to a totipotent state but has poor efficiency in supporting full-term development. H3K9me3 is considered to be an epigenetic barrier to zygotic genomic activation in 2-cell SCNT embryos. However, the mechanism underlying the failure of H3K9me3 reprogramming during SCNT embryo development remains elusive. Here, we perform genome-wide profiling of H3K9me3 in cumulus cell-derived SCNT embryos. We find redundant H3K9me3 marks are closely related to defective minor zygotic genome activation. Moreover, SCNT blastocysts show severely indistinct lineage-specific H3K9me3 deposition. We identify MAX and MCRS1 as potential H3K9me3-related transcription factors and are essential for early embryogenesis. Overexpression of Max and Mcrs1 significantly benefits SCNT embryo development. Notably, MCRS1 partially rescues lineage-specific H3K9me3 allocation, and further improves the efficiency of full-term development. Importantly, our data confirm the conservation of deficient H3K9me3 differentiation in Sertoli cell-derived SCNT embryos, which may be regulated by alternative mechanisms.

2023-07-10 | GSE195762 | GEO

Unreprogrammed H3K9me3 prevents minor zygotic genome activation and lineage commitment in SCNT embryos

2023-07-10 | GSE195760 | GEO