Caenorhabditis elegans
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA236145 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1139590.fastq.gz | Fastqsanger.gz | |||
| SRR1139581.fastq.gz | Fastqsanger.gz | |||
| SRR1139591.fastq.gz | Fastqsanger.gz | |||
| SRR1139582.fastq.gz | Fastqsanger.gz | |||
| SRR1139592.fastq.gz | Fastqsanger.gz |
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Project description:Argonaute-associated siRNAs and Piwi-associated piRNAs have overlapping roles in silencing mobile genetic elements in animals. In C. elegans, mutator-class (mut) genes mediate siRNA-guided repression of transposons as well as exogenous RNA-directed gene silencing (RNAi), but their roles in endogenous RNA silencing pathways are not well understood. To characterize the endogenous small RNAs dependent on mutator-class genes, small RNA populations from a null allele of mut-16, as well as a regulatory mut-16(mg461) allele that disables only somatic RNAi, were subjected to deep sequencing.
2011-02-01 | GSE26165 | GEO
Project description:Argonaute-associated siRNAs and Piwi-associated piRNAs have overlapping roles in silencing mobile genetic elements in animals. In C. elegans, mutator-class (mut) genes mediate siRNA-guided repression of transposons as well as exogenous RNA-directed gene silencing (RNAi), but their roles in endogenous RNA silencing pathways are not well understood. To characterize the endogenous small RNAs dependent on mutator-class genes, small RNA populations from a null allele of mut-16, as well as a regulatory mut-16(mg461) allele that disables only somatic RNAi, were subjected to deep sequencing. Small RNA analysis in wild type and mut-16 mutant C. elegans strains
2011-02-01 | E-GEOD-26165 | biostudies-arrayexpress
Project description:The aim of this experiment was to look at RNAs which associate with DEAD-box RNA helicases with and without 10 minutes of glucose starvation.
2021-09-30 | E-MTAB-9095 | biostudies-arrayexpress
Project description:DDX23 belongs to DEAD-box family of RNA helicases and plays crucial roles in spliceosome formation and pre-mRNA splicing. In this study, DDX23 was first identified as a key DEAD-box RNA helicase in ovarian cancer, and its overexpressed was associated with poor clinical outcomes. High expression of DDX23 was involved in the malignant proliferation and aggressiveness of ovarian cancer.
2021-07-31 | GSE181078 | GEO
Project description:RNA interference (RNAi) is a potent mechanism for down-regulating gene expression. Conserved RNAi pathway components are found in animals, plants, fungi and other eukaryotes. In C. elegans, the RNAi response is greatly amplified by the synthesis of abundant secondary siRNAs. Exogenous double stranded RNA is processed by Dicer and RDE-1/Argonaute into primary siRNA that guides target mRNA recognition. The RDE-10/RDE-11 complex and the RNA dependent RNA polymerase RRF-1 then engage the target mRNA for secondary siRNA synthesis. However, the molecular link between primary siRNA production and secondary siRNA synthesis remains largely unknown. Furthermore, it is unclear if the sub-cellular sites for target mRNA recognition and degradation coincide with sites where siRNA synthesis and amplification occur. In the C. elegans germline, cytoplasmic P granules at the nuclear pores and perinuclear Mutator foci contribute to target mRNA surveillance and siRNA amplification, respectively. We report that RDE-12, a conserved FG domain containing DEAD-box helicase, localizes in P-granules and cytoplasmic foci that are enriched in RSD-6 but are excluded from the Mutator foci. Our results suggest that RDE-12 promotes secondary siRNA synthesis by orchestrating the recruitment of RDE-10 and RRF-1 to primary siRNA targeted mRNA in distinct cytoplasmic compartments. Examination of exogenous dsRNA trigger derived siRNA in wildtype and rde-12 mutant animals
2014-03-27 | E-GEOD-53830 | biostudies-arrayexpress
Project description:RNA interference (RNAi) is a potent mechanism for down-regulating gene expression. Conserved RNAi pathway components are found in animals, plants, fungi and other eukaryotes. In C. elegans, the RNAi response is greatly amplified by the synthesis of abundant secondary siRNAs. Exogenous double stranded RNA is processed by Dicer and RDE-1/Argonaute into primary siRNA that guides target mRNA recognition. The RDE-10/RDE-11 complex and the RNA dependent RNA polymerase RRF-1 then engage the target mRNA for secondary siRNA synthesis. However, the molecular link between primary siRNA production and secondary siRNA synthesis remains largely unknown. Furthermore, it is unclear if the sub-cellular sites for target mRNA recognition and degradation coincide with sites where siRNA synthesis and amplification occur. In the C. elegans germline, cytoplasmic P granules at the nuclear pores and perinuclear Mutator foci contribute to target mRNA surveillance and siRNA amplification, respectively. We report that RDE-12, a conserved FG domain containing DEAD-box helicase, localizes in P-granules and cytoplasmic foci that are enriched in RSD-6 but are excluded from the Mutator foci. Our results suggest that RDE-12 promotes secondary siRNA synthesis by orchestrating the recruitment of RDE-10 and RRF-1 to primary siRNA targeted mRNA in distinct cytoplasmic compartments.
2014-03-27 | GSE53830 | GEO
Project description:Chromatin-associated RNAs have diverse roles in the nucleus. However, their mechanisms of action are poorly understood, in part due to the inability to identify proteins that specifically associate with chromatin-bound RNAs. Here, we address this problem for a subset of chromatin-associated RNAs that form R-loops—RNA-DNA hybrid structures that include a displaced strand of single-stranded DNA. R-loops generally form co-transcriptionally and have important roles in regulation of gene expression, immunoglobulin class switching, and other processes. However, unresolved R-loops can lead to DNA damage and chromosome instability. To identify factors that may bind and potentially regulate R-loop accumulation or mediate R-loop-dependent functions, we used a comparative immunoprecipitation/mass spectrometry approach, with and without RNA-protein crosslinking, to identify a stringent set of R-loop-binding proteins in mouse embryonic stem cells. We identified 365 R-loop-interacting proteins, which were highly enriched for proteins with predicted RNA-binding functions. We characterized several R-loop-interacting proteins of the DEAD-box family of RNA helicases and found that these proteins localize to the nucleolus and, to a lesser degree, the nucleus. Consistent with their localization patterns, we found that these helicases are required for ribosomal RNA processing and regulation of gene expression. Surprisingly, depletion of these helicases resulted in misregulation of highly overlapping sets of protein-coding genes, including many genes that function in differentiation and development. We conclude that R-loop-interacting DEAD-box helicases have non-redundant roles that are critical for maintaining the normal embryonic stem cell transcriptome.
2021-09-17 | PXD022697 | Pride
Project description:DEAD box (DDX) RNA helicases are a large family of ATPases, many of which have unknown functions. There is emerging evidence that besides their role in RNA biology, DDX proteins may stimulate protein kinases. To investigate if protein kinase-DDX interaction is a more widespread phenomenon, we conducted three orthogonal large-scale screens, including proteomics analysis with 32 RNA helicases, protein array profiling, and kinome-wide in vitro kinase assays. We retrieved Ser/Thr protein kinases as prominent interactors of RNA helicases and report hundreds of binary interactions. We extracted members of eleven protein kinase families, which bind to - and are stimulated by - DDX proteins, including CAMK, CDK, CK1, CK2, DYRK, MARK, NEK, PRKC, SPRK, STE7/MAP2K, and STE20/PAK family members. We identified MARK1 in all screens and validated that DDX proteins accelerate MARK1 catalytic rate. The findings indicate pervasive interactions between protein kinases and DEAD box RNA helicases and provide a rich resource to explore their regulatory relationships.
2024-03-10 | PXD043289 | Pride
Project description:Transcriptional profiling of HT29 colon cancer cells comparing siRNA-targeted knockdowns of glutaminase (GLUT), cytokeratin 20 (KER), DEAD/H box polypeptide 32 (DEAD), ribosomal protein L32 (RPL32) and transcription factor DP1 (TFDP1) versus scrambled siRNA control and GFP siRNA control Keywords: two-color spotted cDNA microarray, siRNA-targeted gene knockdowns
2008-06-21 | GSE11848 | GEO
Project description:Background: Causative genes are mostly unknown for the mismatch repair-proficient category of familial colorectal cancers designated as FCCTX. Recent evidence suggests shared susceptibility factors between colorectal and hematological malignancies. Study design: We investigated 28 FCCTX families by exome sequencing, supplemented with whole genome sequencing, RNA-sequencing, and tumor studies to identify the predisposing genes. Guided by the findings, germline and somatic exomes of ~400 patients with acute leukemia, myelodysplastic syndrome, and myeloma were subsequently examined. Results: A family with hematological and solid malignancies revealed a truncating variant in the DEAH-box RNA helicase gene DHX40 co-segregating with disease in seven family members. Neoplastic tissues revealed no apparent “second hit”, implying a haploinsufficiency model of tumorigenesis. DHX40 siRNA-treated cell lines exhibited a 13% increase in aberrantly spliced transcripts vs. GAPDH-siRNA or non-target siRNA-treated cells. Two additional families showed truncating germline variants in the TDRD9 and TDRD5 genes encoding Tudor domain-containing RNA-binding proteins. In the hospital-based hematological series, 18% of germline and 28% of somatic exomes revealed possibly pathogenic DEAD/H box gene variants, including somatic variants of DHX40 in four. Conclusions: This study identifies DHX40, TDRD9, and TDRD5 as novel candidate genes for FCCTX predisposition. In the family segregating the truncating DHX40 variant, two carriers had hematological neoplasia, suggesting possible analogy to DDX41, a DEAD-box RNA helicase gene previously linked to myeloid malignancies. Our findings emphasize aberrant RNA metabolism behind FCCTX and hematological neoplasia.
2023-11-08 | GSE228991 | GEO