Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

E-MTAB-5210

ABSTRACT: Transcription profiling of wild type and Stella knockout oocytes, wild type and Stella maternal/zygotic knockout embryos to study to the role of Stella in early mouse development

PROVIDER: E-MTAB-5210 | ExpressionAtlas | 2019-05-14

REPOSITORIES: ExpressionAtlas

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	E-MTAB-5210-analysis-methods.tsv	Tabular
	E-MTAB-5210-analytics.tsv	Tabular
	E-MTAB-5210-atlasExperimentSummary.Rdata	Rdata
	E-MTAB-5210-configuration.xml	Xml
	E-MTAB-5210-g2_g1-mvaPlot.png	Other

Items per page:

1 - 5 of 41

Similar Datasets

Gene expression changes in GADD45 deficient 2-cell mouse embryos

Project description:To study the role of GADD45 proteins in early mouse development, RNA-seq expression profiling was performed with Gadd45a/Gadd45b double knockout (DKO) and wild-type (WT) mouse embryos at 2-cell stage (2C).

2019-05-31 | GSE127719 | GEO

STELLA and MuERV-L activation are essential for early mouse development

Project description:The maternal-to-zygotic transition (MZT) marks the period when the embryonic genome is activated and acquires control of development. Maternally inherited factors play a key role in this critical developmental process, which occurs at the 2-cell stage in mice. Here we investigated the function of the maternally inherited factor STELLA (DPPA3) using single-cell/embryo approaches. This submission concerns itself with transcriptional profiling of wild type and Stella knockout (Stella-/-) oocytes, wild type and Stella maternal/zygotic knockout (StellaM/Z-/-) 1-cell and 2-cell embryos. We show that loss of maternal STELLA results in widespread transcriptional mis-regulation and a partial failure of MZT. Strikingly, activation of the LTR class of transposable elements (TE), and particularly 2-cell specific MuERV-L elements, is significantly impaired in StellaM/Z-/- embryos, which leads to a failure to upregulate selected chimeric transcripts. We propose that STELLA is involved in ensuring activation of TEs that themselves play a key role during early development, in part through regulating embryonic gene expression.

2017-03-22 | E-MTAB-5210 | biostudies-arrayexpress

Maternal MicroRNAs are Essential for Mouse Zygotic Development

Project description:MicroRNAs (miRNAs) have been shown to have important functions in a variety of cellular processes. Here we report on miRNA expression and their dynamic regulation during mouse oogenesis and early embryos. We show that following specific deletion of Dicer from growing oocytes, the mutant oocytes cease development and were unable to progress through the first cell division. While the mutant mature oocytes seemed morphologically normal, they had disorganized spindle. Using detailed single cell cDNA microarray analysis of normal versus mutant oocytes, we found that a large proportion of maternal genes, including C-mos, are under the control of miRNAs. This study provides strong evidence that maternal miRNAs are essential for the earliest stages of mouse embryonic development. mRNA expression was compared with miRNA expression in dicer knockout and wild-type mouse mature oocyte.

2010-06-11 | E-GEOD-6806 | biostudies-arrayexpress

Maternal Plag1 deficiency delays two-cell stage embryo development and embryonic genome activation [Embryos]

Project description:Pleomorphic adenoma gene 1 (PLAG1) encodes a transcription factor involved in cancer and growth. We study the role of PLAG1 in preimplantation embryos using STRT RNA-seq of single embryos from wild type and knockout mothers (both mated with wild type studs). The lack of maternal Plag1 led to delayed mouse 2-cell stage embryo development, compensatory expression of Plag1 from the paternal allele, and dysregulation of 1,089 genes. Half of these genes displayed a pattern of delayed activation and play roles in ribosome biogenesis and protein synthesis. These mouse genes further showed a significant overlap with human EGA genes with similar ontology, and an enrichment of the PLAG1 de novo motif. We conclude that Plag1 affects EGA through retrotransposons influencing ribosomes and protein synthesis, a mechanism that might also explain its roles in cancer and growth

2019-06-20 | GSE111039 | GEO

Transcriptome analysis of wild-type and maternal ybx1 mutant zebrafish embryos during early development

Project description:To study the function of zebrafish Ybx1 during early embryogenesis, we generated maternal ybx1 (Mybx1) mutant using CRISPR/Cas9 and report the transcriptome-wide changes in comparison to wild-type (WT) embryos. Our analysis reveals a dramatic loss of maternal mRNA decay and zygotic genome activation in Mybx1 embryos during maternal-to-zygotic transition.

2018-09-01 | GSE108924 | GEO

Maternal Plag1 deficiency delays two-cell stage embryo development and embryonic genome activation [Uterus]

Project description:Pleomorphic adenoma gene 1 (PLAG1) encodes a transcription factor involved in cancer and growth. We study the role of PLAG1 in female reproductive tract and preimplantation embryos using STRT RNA-seq of single embryos from wild type and knockout mothers (both mated with wild type studs). We did not find significant effects in ovaries or uterus. The lack of maternal Plag1 led to delayed mouse 2-cell stage embryo development, compensatory expression of Plag1 from the paternal allele, and dysregulation of 1,089 genes. Half of these genes displayed a pattern of delayed activation and play roles in ribosome biogenesis and protein synthesis. These mouse genes further showed a significant overlap with human EGA genes with similar ontology, and an enrichment of the PLAG1 de novo motif. We conclude that Plag1 affects EGA through retrotransposons influencing ribosomes and protein synthesis, a mechanism that might also explain its roles in cancer and growth

2019-06-20 | GSE111035 | GEO

Transcriptome analysis of wild-type and maternal ybx1 mutant zebrafish embryos during early development

Project description:Transcriptome analysis of wild-type and maternal ybx1 mutant zebrafish embryos during early development

| PRJNA429172 | ENA

Protein expression profiling in eggs and embryos from control and Eif4e1b knockout female mice.

Project description:We have identified eukaryotic translation initiation factor 4E family member 1B (Eif4e1b) as a regulator of maternal RNA translation, whose maternal deletion leads to 2-cell arrest phenotype in mouse embryos. eIF4E1b protein binds mRNA selectively in oocytes and controls their translation in early embryos. We aim to profile the global changes in protein expression in metaphase II (MII) eggs and zygotes collected from control or Eif4e1b knockout female mice. An encapsulated proteomic-sample processing protocol is used to perform this low-input mass spectrometry to quantify proteomic changes (Kulak et al. 2014/PMID 24497582).

2023-06-12 | PXD041583 | Pride

Maternal protein rbpms2 play a crucial role in mouse blastocyst formation

Project description:The functional role of the maternal protein during early embryo development remains to be elucidated. Here we show that the maternal protein, Rbpms2, is highly expressed in mouse oocytes and that knockdown of Rbpms2 inhibits development from the morula to blastocyst stage. To study the underlying mechanism, we firstly analysed the differential expressed genes after Rbpms2 knockdown through single-cell sequencing. Combined the bioinformatics analysis of sequencing data, we then identify the impaired location of E-cadherin after knockdown of Rbpms2 may leading to the morula arrested development . Furthermore, Rbpms2 is important for development of mouse early embryos, most likely because it activates the BMP pathway. Taken together, our study uncovers that Rbpms2 activate the BMP pathway, and thus adjust the location of E-cadherin which is important for mouse early embryos development.

2023-06-21 | GSE202359 | GEO

Haploinsufficiency, but not defective paternal 5mC oxidation, accounts for the developmental defects of maternal Tet3 knockouts

Project description:DNA demethylation of paternal genome in zygotes takes place in various mammals including mice and human. Recent studies have revealed that this is achieved through Tet3-mediated iterative oxidation of 5-methylcytosine (5mC) coupled with replication-dependent dilution. Tet3-mediated paternal DNA demethylation is believed to be required for mouse development given that Tet3 heterozygous embryos, derived by fertilizing Tet3 knockout (KO) oocytes with wild-type (WT) sperms, exhibit 5mC oxidation defects and embryonic sublethality, Here we demonstrate that the sublethality phenotype of the maternal KO mice is caused by haploinsufficiency of Tet3, but not by defective paternal 5mC oxidation. We found that Tet3 heterozygous mice derived from crosses of heterozygous father or mother with WT mice also exhibit sublethality phenotype similarly to Tet3 maternal KO mice. Importantly, embryos reconstituted with WT paternal nuclei that bypassed 5mC oxidation develop to term and grow to adulthood normally. Genome-scale DNA methylation analysis of the maternal KO zygotes and blastocysts demonstrated that hypermethylation caused by the depletion of maternal Tet3 is largely diminished by the blastocyst stage. Our study thus not only demonstrates that Tet3-mediated paternal 5mC oxidation is dispensable for mouse development but also suggests the existence of a compensation mechanism in preimplantation embryos that can compensate for the defective 5mC oxidation in zygotes. This data set includes RRBS data of wild-type and maternal Tet3 KO zygotes and blastocysts (C57BL/6J x CAST/EiJ)

2015-02-28 | E-GEOD-62719 | 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