Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

MRNA transcriptome analysis of Ddx6 knockout embryos

ABSTRACT: DDX6 is an RNA helicase and involved in various post-transcriptional regulatory processes. Although DDX6 is an evolutionarily well conserved central player in post-transcriptional gene regulation, its function in embryonic development remains obscure. To study this, we examined Ddx6 knockout mouse embryos and pluripotent cell lines. E8.5 Ddx6 mutants exhibited gastrulation defects. To transcriptomically identify the existing cell population in E8.5 mutant embryos and further find the possible causes of this defect, we performed RNA-seq analysis with E8.5 embryo cDNA libraries.

ORGANISM(S): Mus musculus

PROVIDER: GSE171156 | GEO | 2022/08/22

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

mRNA transcriptome analyses of the functions of DDX6-mediated pathways during EpiLC induction

Project description:DDX6 is an RNA helicase and involved in various post-transcriptional regulatory processes. Although DDX6 is an evolutionarily well conserved central player in post-transcriptional gene regulation, its function in embryonic development remains obscure. In this study, we have identified the crucial functions of DDX6 during early mouse embryogenesis. However, due to its wide range of involvement, the more detailed dissection of DDX6-mediated functions was required to pinpoint which specific DDX6 function is important. For this purpose, we selected a key gene of each well-known DDX6 pathway, generated KO ES line, then made cDNA libraries of ESC and EpiLC Day2 samples to investigate transcriptomic differences during the very early differentiation processes of embryonic pluripotent cells.

2022-08-22 | GSE187390 | GEO

RNA-seq of coding RNA from DDX6 knockout human haploid (HAP1) cells

Project description:We performed a genome-scale screen for suppressors of interferon stimulated gene (ISG) expression in human haploid cells (HAP1). DEAD-box helicase 6 (DDX6) was a significant hit. In order to validate DDX6 as a regulator of ISG expression, we created knockouts of DDX6 in HAP1 cells using CRISPR-Cas9 and performed RNA-seq on coding RNA from DDX6 KO and WT cells. This data was used to determine if ISGs were upregulated in DDX6 KO HAP1 cells.

2017-07-25 | E-MTAB-5867 | biostudies-arrayexpress

Large-scale study of total and polysomial mRNA after DDX6 depletion in HEK293 cells

Project description:DDX6 is an abundant cytoplasmic DEAD-box RNA helicase which is involved in disparate aspects of mRNA stability and translation, leading to a confused understanding of its global function. We carried out a large-scale study of total and polysomial mRNA after DDX6 depletion to get an accurate picture of its roles in human cells.

2017-09-28 | E-MTAB-4091 | biostudies-arrayexpress

The RNA helicase DDX6 regulates self-renewal and differentiation of human and mouse stem cells [RNA-seq2]

Project description:Post-transcriptional mechanisms have the potential to influence complex changes in gene expression, yet their role in cell fate transitions remain largely unexplored. Here, we show that the RNA helicase DDX6 is crucial for the dissolution of the pluripotency-specific transcriptional network in mouse and human embryonic stem cells (ESCs). We further demonstrate that epigenetic silencing of DDX6 endows primed ESCs with a differentiation-resistant, “hyper-pluripotent” state, which readily reprograms to a naïve state resembling the preimplantation embryo. In addition to directing cell fate in ESCs, we find that DDX6 plays a key role in adult progenitors where it controls the balance between self-renewal and differentiation in a context-dependent manner. Specifically, DDX6 loss blocks the differentiation of mouse intestinal stem cells and human neural stem cells, while it favors exit from the progenitor state in human muscle and mesenchymal progenitors. Mechanistically, we show that DDX6 coordinates the storage and translational suppression of target mRNAs in P-bodies. Upon loss of DDX6 or mutation of its helicase domain, P-bodies dissolve and release mRNAs encoding fate-instructive transcription and chromatin factors that subsequently re-enter the ribosome pool. Increased translation of these targets impacts cell fate by rewiring the enhancer, heterochromatin and DNA methylation landscapes of human undifferentiated cell types. Collectively, our data establish a novel link between P-body homeostasis, chromatin organization and cellular potency across diverse stem and progenitor cell populations.

2019-10-16 | GSE134164 | GEO

Human DDX6 regulates translation and decay of inefficiently translated mRNAs

Project description:Recent findings indicate that the translation elongation rate influences mRNA stability. One of the factors that has been implicated in this link between mRNA decay and translation speed is the yeast DEAD-box helicase Dhh1p. Here, we demonstrate that the human ortholog of Dhh1p, DDX6, triggers deadenylation-dependent decay of inefficiently translated mRNAs in human cells. DDX6 interacts with the ribosome through the Phe-Asp-Phe (FDF) motif in its RecA2 domain. Furthermore, RecA2-mediated interactions and ATPase activity are both required for DDX6 to destabilize inefficiently translated mRNAs. Using ribosome profiling and RNA sequencing, we identified two classes of endogenous mRNAs that are regulated in a DDX6-dependent manner. The identified targets are either translationally regulated or regulated at the steady-state-level and either exhibit signatures of poor overall translation or of locally reduced ribosome translocation rates. Transferring the identified sequence stretches into a reporter mRNA caused translation- and DDX6-dependent degradation of the reporter mRNA. In summary, these results identify DDX6 as a crucial regulator of mRNA translation and decay triggered by slow ribosome movement and provide insights into the mechanism by which DDX6 destabilizes inefficiently translated mRNAs.

2024-01-23 | GSE231964 | GEO

mRNA transcriptome analysis of Ddx6 knockout embryos

Project description:mRNA transcriptome analysis of Ddx6 knockout embryos

| PRJNA718566 | ENA

Specific Interaction of DDX6 with an RNA Hairpin in the 3?-UTR of the Dengue Genome Mediates G1 Phase Arrest

Project description:The extent to which viral genomic RNAs interact with host factors and contribute to host response and disease pathogenesis is not well known. Here, we report that the human RNA helicase DDX6 specifically binds to the viral most conserved RNA hairpin in the A3 element in the dengue 3´-UTR, with nanomolar affinities. DDX6 CLIP confirmed the interaction in HuH-7 cells infected by dengue virus serotype 2. This interaction requires three conserved residues, Lys307, Lys367, and Arg369, as well as the unstructured extension in the C-terminal domain of DDX6. Interestingly, alanine substitution of these three basic residues resulted in RNA-independent ATPase activity, suggesting a mechanism by which RNA-binding and ATPase activities are coupled in DEAD-box helicases. Furthermore, we applied a cross-omics gene enrichment approach to suggest that DDX6 is functionally related to cell cycle regulation and viral pathogenicity. Indeed, infected cells exhibited cell cycle arrest in G1 phase and a decrease in the early S phase. Exogeneous expression of intact DDX6, but not A3-binding-deficient mutants, alleviated these effects by rescue of the DNA pre-initiation complex expression. Disruption of the DDX6-binding site was found in dengue and Zika live-attenuated vaccine strains. Our results suggested that dengue virus has evolved an RNA aptamer against DDX6 to alter host cell states, and defined DDX6 as a new regulator of G1/S transition.

2021-06-10 | GSE169526 | GEO

Specific Interaction of DDX6 with an RNA Hairpin in the 3´-UTR of the Dengue Genome Mediates G1 Phase Arrest

2021-06-10 | GSE142605 | GEO

miR-148a-3p and DDX6 functional link promotes survival of myeloid leukemia cells

Project description:Post-transcriptional regulation of genes is heavily dependent on the action of miRNAs. miRNAs take part in various cellular processes and have been shown to be crucial in oncogenesis. Identification of miRNA targets is crucial for understanding its functions in different cellular contexts. miR-148a-3p is highly expressed in HCT116 cells and several other cell lines. However, the studies about mRNA targetting activitiy of this miRNA was limited. In this study, we aimed at identifying target repotoire of miR-148a-3p by using HCT116 DROSHA-KO model. We found several genes that are under miR-148a-3p regulation, including several reported targets. We next found the negative association between miR-148a-3p and DDX6, one of the identified gene, in leukemia. We examined DDX6 functions in this cancer and showed that the depletion of DDX6 helps impair leukemia cell growth, promote apoptosis and increase survival rate of transplanted mice. We then identified that DDX6 functions to suppress TXNIP, a well known tumor suppressor in leukemia and various types of cancer. Our findings uncovered the regulation axis between miR-148a-3p/DDX6/TXNIP in leukemia which provides molecular mechanism basis for therapeutic treatment directions.

2022-06-07 | GSE201905 | GEO

The RNA helicase DDX6 regulation in human skeletal myoblasts [eCLIP-seq]

Project description:The RNA helicase DDX6 regulation in human skeletal myoblasts [eCLIP-seq]

| PRJNA517602 | ENA