Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ABSTRACT: Maternal Plag1 deficiency delays two-cell stage embryo development and embryonic genome activation

PROVIDER: PRJNA435674 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR6765740.fastq.gz	Fastqsanger.gz
	SRR6765750.fastq.gz	Fastqsanger.gz
	SRR6765760.fastq.gz	Fastqsanger.gz
	SRR6765770.fastq.gz	Fastqsanger.gz
	SRR6765780.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 135

Similar Datasets

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

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

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

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

| PRJNA435677 | ENA

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

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

| PRJNA435667 | ENA

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

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

2019-06-20 | GSE111040 | GEO

Plag1 in the mouse Epididymis

Project description:RNA sequencing of Plag1 mouse epididymides. 5 each of Plag1 WT, HET and KO whole epididymis tissues were sequenced.

2019-11-19 | GSE140576 | GEO

Plag1 overexpression cooperates with Evi1 overexpression and Gata1s mutation in leading to M7 leukemia

Project description:The goal of this study is to develop a Plag1 signature and determine how its overexpression contributes to leukemogenesis. To study this, we transduced an immortalized (but not transformed) cell line (derived from Gata1s mutant fetal liver progenitor through insertional mutagenesis) by Plag1-expressing retrovirus. This turned a non-transformed cell line to a leukemogenic cell line. To study whether Plag1 overexpression led to deregulation of signaling pathways that may contribute to leukemic transformation, we generated microarray gene expression profiles of this cell line transduced with either Plag1 or the empty vector. We generated gene expression profiles by microarray from stable cell lines transduced with either the empty vector or the Plag1-expressing vector.

2010-08-01 | E-GEOD-16679 | biostudies-arrayexpress

Plag1 overexpression cooperates with Evi1 overexpression and Gata1s mutation in leading to M7 leukemia

2010-08-01 | GSE16679 | GEO

RNA-seq of Lin-CD34+ cord-blood cells expressing shRNA against PLAG1 or control [KD]

Project description:To characterize transcriptional changes associated with loss of the transcription factor PLAG1-S that could contribute to PLAG1 essentiality in long-term human HSC we performed RNA-seq of 2 pools of Lin-CD34+ cord-blood derived hematopoietic stem and progenitor cells 72 hours following lentiviral introduction of shRNA against PLAG1 or non-targeting control.

2022-12-01 | GSE181991 | GEO

Maternal Smchd1 regulates Hox gene expression and patterning in the mouse embryo [RNAseq mESC]

Project description:Parents transmit genetic and epigenetic information to their offspring. Maternal effect genes regulate the offspring epigenome to ensure normal development. Here we report that the epigenetic regulator SMCHD1 has a maternal effect on Hox gene expression and skeletal patterning. Maternal SMCHD1, present in the oocyte and preimplantation embryo, prevents precocious activation of Hox genes post-implantation. Without maternal SMCHD1, highly penetrant posterior homeotic transformations occur in the embryo. Hox genes are decorated with Polycomb marks H2AK119ub and H3K27me3 from the oocyte throughout early embryonic development; however, loss of maternal SMCHD1 does not deplete these marks. Therefore, we propose maternal SMCHD1 acts downstream of Polycomb marks to establish a chromatin state necessary for persistent epigenetic silencing and appropriate Hox gene expression later in the developing embryo. This is a striking role for maternal SMCHD1 in long-lived epigenetic effects impacting offspring phenotype.

2022-06-27 | GSE183736 | GEO

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