Ontology highlight
ABSTRACT:
PROVIDER: PRJNA112471 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR015056.fastq.gz | Fastqsanger.gz | |||
| SRR015057.fastq.gz | Fastqsanger.gz | |||
| SRR015058.fastq.gz | Fastqsanger.gz | |||
| SRR015059.fastq.gz | Fastqsanger.gz | |||
| SRR015060.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 14 |
Similar Datasets
Project description:When C. elegans larvae hatch in the absence of food they persist in a stress resistant, developmentally arrested state (L1 arrest) for weeks or until food becomes available. We characterized growth, mRNA expression, and RNA Polymerase II activity genome-wide during L1 arrest and recovery. RNA Pol II binding data resulting from ChIP-Seq experiments using the Illumina Genome Analyzer are included in this GEO submission. Complementary mRNA expression data from the Affymetrix microarray platform can be found at GEO accession# GSE11055. The goals of the Pol II ChIP-Seq compononent of this project were to use Pol II antibodies 1) to investigate patterns of transcription in developmentally arrested larvae, when mRNA expression levels have reached steady state; 2) to investigate patterns of transcription in immediate response to feeding, when mRNA expression levels change dramatically; and 3) to investigate accumulation of Pol II at promoters during arrest and recovery. We started our ChIP studies with the S2 antibody (Abcam ab5095) since it was raised against a Ser2 phosphorylated peptide from the C-terminal domain of Pol II and should therefore be relatively specific for active, elongating Pol II, and it worked well for the first two goals above. In order to investigate accumulation of Pol II at promoters, we used the S2 antibody and complemeted it with antibody 4H8 (Abcam ab5408), which according to the manafacturer recognizes phosphorylated and non-phosphorylated Pol II, and antibody 8WG16 (Abcam ab817), which binds primarily to non-phosphorylated Pol II but also relatively weakly to phosphorylated Pol II. We were somewhat surprised to find that the results obtained with each of these antibodies were very similar, though upon deeper analysis we discovered relatively subtle differences consistent with the relative specificities of each antibody and existing models regarding phosphorylation state of Pol II and its activity and location. In summary, we find that while Pol II continues transcribing starvation genes, it is M-bM-^@M-^XpausedM-bM-^@M-^Y accumulates on the promoters of growth and development genes during L1 arrest. Consistent with it poising arrested larvae for recovery, pausingpromoter accumulation decreases in response to feeding, while elongation and mRNA levels increase. These results demonstrate that Pol II pausing is widespread in C. elegans and that it is nutritionally controlled during development.These results demonstrate that accumulation of Pol II at promoters of growth and development genes is common in C. elegans and that promoter accumulation anticipates nutritionally controlled gene expression during development. RNA Pol II binding was examined with three different antibodies (S2, 4H8, and 8WG16) during either L1 arrest (starvation) or after 1 hr recovery by feeding. For the S2 antibody two different time points during L1 arrest were examined (6 and 12 hr). 14 total samples are included: 4 independent control samples (Input), a pair biological replicates with the S2 antibody at 6 hr L1 arrest, a pair of biological replicates with the 4H8 antibody at 12 hr L1 arrest and at 1 hr recovery, and singletons for the S2 and 8WG16 antibodies at 12 hr L1 arrest and at 1 hr recovery. "GSE13973_PolII_ChIP-Seq.xls.gz" contains 5 worksheets with the following contents: "geneDensity" includes the number of reads per million mapping to each gene model normalized to gene length. Units are reads per million per kilobase. "TSSdensity" includes the number of reads per million mapping to a 200 bp window spanning the most upstream transcription start site for each gene and normalized by length (200 bp). Units are reads per million per kilobase. "geneEnrichment" includes the fold-enrichment of read density over each gene model relative to input. Where input values were below the median of all input values then the median was used. Units are fold-enrichment. "TSSenrichment" includes the fold-enrichment of read density over the 200 bp TSS window relative to input. Where input values were below the median of all input values then the median was used. Units are fold-enrichment. "5' bias" includes 5' bias calculation for each gene and each antibody in each condition. "GSE13973_CelegansWS190_GeneCoordinates.xls.gz" contains the gene coordinates based on version WS190 of the C. elegans genome.
2009-02-27 | E-GEOD-13973 | biostudies-arrayexpress
Project description:When C. elegans larvae hatch in the absence of food they persist in a stress resistant, developmentally arrested state (L1 arrest) for weeks or until food becomes available. We characterized growth, mRNA expression, and RNA Polymerase II activity genome-wide during L1 arrest and recovery. RNA Pol II binding data resulting from ChIP-Seq experiments using the Illumina Genome Analyzer are included in this GEO submission. Complementary mRNA expression data from the Affymetrix microarray platform can be found at GEO accession# GSE11055. The goals of the Pol II ChIP-Seq compononent of this project were to use Pol II antibodies 1) to investigate patterns of transcription in developmentally arrested larvae, when mRNA expression levels have reached steady state; 2) to investigate patterns of transcription in immediate response to feeding, when mRNA expression levels change dramatically; and 3) to investigate accumulation of Pol II at promoters during arrest and recovery. We started our ChIP studies with the S2 antibody (Abcam ab5095) since it was raised against a Ser2 phosphorylated peptide from the C-terminal domain of Pol II and should therefore be relatively specific for active, elongating Pol II, and it worked well for the first two goals above. In order to investigate accumulation of Pol II at promoters, we used the S2 antibody and complemeted it with antibody 4H8 (Abcam ab5408), which according to the manafacturer recognizes phosphorylated and non-phosphorylated Pol II, and antibody 8WG16 (Abcam ab817), which binds primarily to non-phosphorylated Pol II but also relatively weakly to phosphorylated Pol II. We were somewhat surprised to find that the results obtained with each of these antibodies were very similar, though upon deeper analysis we discovered relatively subtle differences consistent with the relative specificities of each antibody and existing models regarding phosphorylation state of Pol II and its activity and location. In summary, we find that while Pol II continues transcribing starvation genes, it is ‘paused’ accumulates on the promoters of growth and development genes during L1 arrest. Consistent with it poising arrested larvae for recovery, pausingpromoter accumulation decreases in response to feeding, while elongation and mRNA levels increase. These results demonstrate that Pol II pausing is widespread in C. elegans and that it is nutritionally controlled during development.These results demonstrate that accumulation of Pol II at promoters of growth and development genes is common in C. elegans and that promoter accumulation anticipates nutritionally controlled gene expression during development.
2009-02-27 | GSE13973 | GEO
Project description:We show that inactivating CDK-12 or expressing a full-length CTD S2A mutant in Caenorhabditis elegans results in developmental arrest at the L1 stage,which mimicks the diapause induced when hatching occurs in the absence of food. Transcriptomic analyses indicate that when CDK-12 is inhibited, only a subset of growth-related genes is not properly expressed. These genes correspond to SL2 trans-spliced mRNAs located in position 2 and over within operons. We show that CDK-12 is required for maximal occupancy of CstF (cleavage stimulatory factor) required for SL2 trans-splicing. The addition of food to developmentally arrested worms leads to an increase of both CTD S2P and SL2 trans-splicing. We propose that CTD S2P functions as a gene-specific signaling mark ensuring the nutritional control of C. elegans development.
2020-10-20 | GSE145456 | GEO
Project description:RAD-seq of C. elegans wild isolates during L1 arrest
| PRJNA533789 | ENA
Project description:We show that inactivating CDK-12 or expressing a full-length CTD S2A mutant in Caenorhabditis elegans results in developmental arrest at the L1 stage,which mimicks the diapause induced when hatching occurs in the absence of food. Transcriptomic analyses indicate that when CDK-12 is inhibited, only a subset of growth-related genes is not properly expressed. These genes correspond to SL2 trans-spliced mRNAs located in position 2 and over within operons. We show that CDK-12 is required for maximal occupancy of CstF (cleavage stimulatory factor) required for SL2 trans-splicing. The addition of food to developmentally arrested worms leads to an increase of both CTD S2P and SL2 trans-splicing. We propose that CTD S2P functions as a gene-specific signaling mark ensuring the nutritional control of C. elegans development.
2020-10-20 | GSE145457 | GEO
Project description:(Part 1) Gene expression profiles of C. elegans in response to a 120 hour S. enterica infection. Synchronized larval stage 1 (L1) animals were exposed to S. enterica SL1344 for 36, 72, 96, or 120 hours. As an uninfected control, synchronized L1 animals were exposed to E. coli OP50 for 36 hours. (Part 2) Gene expression profiles of C. elegans in response to Tetracycline-mediated recovery from 72 hour and 96 hour S. enterica infections. Synchronized L1 animals were exposed to S. enterica SL1344 for 72 hours and then shifted to E. coli HT115 plus Tetracycline plates for 24 hours to resolve the infection. Synchronized L1 animals were exposed to S. enterica SL1344 for 96 hours and then shifted to E. coli HT115 plus Tetracycline plates for 24 hours to resolve the infection.
2014-07-26 | GSE54212 | GEO
Project description:Nutritional intake influences animal growth, reproductive capacity, and survival of animals. Under nutrition deficiency, animal developmental arrest occurs as an adaptive strategy to survive. However, the nutritional basis and the underlying nutrient sensing mechanism essential for animal regrowth after developmental arrest remain to be explored. In Caenorhabditis elegans, larvae undergo early developmental arrest are stress resistant, and they require certain nutrients to recover postembryonic development. Here, we investigated the developmental arrest in C. elegans feeding on Lactiplantibacillus plantarum, and the rescue of the diapause state with trace supplementation of Escherichia coli. We performed a genome-wide screen using 3983 individual gene deletion E. coli mutants and identified E. coli genes that are indispensable for C. elegans larval growth on originally not nutritionally sufficient bacteria L. plantarum. Among these crucial genes, we confirmed E. coli pdxH, and the downstream metabolite pyridoxal 5-P (PLP, Vitamin B6) as important nutritional factors for C. elegans postembryonic development. Transcriptome results suggest that bacterial pdxH affects host development by coordinating host metabolic processes and PLP binding. Additionally, the developmental arrest induced by the L. plantarum diet in worm does not depend on the activation of FoxO/DAF-16. Altogether, these results highlight the role of microbial metabolite PLP as a crucial cofactor to restore postembryonic development in C. elegans.
2024-02-23 | GSE254343 | GEO
Project description:ChIP-Seq of RNA Pol II with antibodies S2, 4H8 and 8WG16 during C. elegans L1 arrest and recovery
| PRJNA114599 | ENA
Project description:(Part 1) Gene expression profiles of C. elegans in response to a 120 hour S. enterica infection. Synchronized larval stage 1 (L1) animals were exposed to S. enterica SL1344 for 36, 72, 96, or 120 hours. As an uninfected control, synchronized L1 animals were exposed to E. coli OP50 for 36 hours. (Part 2) Gene expression profiles of C. elegans in response to Tetracycline-mediated recovery from 72 hour and 96 hour S. enterica infections. Synchronized L1 animals were exposed to S. enterica SL1344 for 72 hours and then shifted to E. coli HT115 plus Tetracycline plates for 24 hours to resolve the infection. Synchronized L1 animals were exposed to S. enterica SL1344 for 96 hours and then shifted to E. coli HT115 plus Tetracycline plates for 24 hours to resolve the infection. Samples include 36 hours on OP50 (36hOP), 36 hours on SL1344 (36hSL), 72 hours on SL1344 (72hSL), 96 hours on SL1344 (96hSL), 120 hours on SL1344 (120hSL), 72 hours on SL1344 plus 24 hours on HT115-Tet (96hHT), 96 hours on SL1344 plus 24 hours on HT115-Tet (120hHT). Duplicate biological samples were included for each timepoint. 14 total samples. Agilent C. elegans expression microarray (GPL14144).
2014-07-26 | E-GEOD-54212 | biostudies-arrayexpress
Project description:Post-embryonic development of the nematode C. elegans is governed by nutrient availability. L1-stage larvae remain in a state of developmental arrest after hatching until they feed. This “L1 arrest” (or "L1 diapause") is associated with increased stress resistance, supporting starvation survival. Loss of the transcription factor daf-16/FOXO, an effector of insulin/IGF signaling, results in arrest-defective and starvation-sensitive phenotypes. We show that daf-16/FOXO regulates L1 arrest cell-nonautonomously, suggesting that insulin/IGF signaling regulates at least one additional signaling pathway. We used mRNA-seq to identify candidate signaling molecules affected by daf-16/FOXO during L1 arrest. daf-16/FOXO had overlapping but distinct effects on gene expression in L1 arrest compared to daf-2/InsR adults. Notably, dbl-1/TGF-β, a ligand for the Sma/Mab pathway, and daf-36, which encodes an upstream component of the daf-12/NHR steroid hormone signaling pathway, were up-regulated during L1 arrest in a daf-16/FOXO mutant. Using genetic epistasis analysis, we show that dbl-1/TGF-β and daf-12/NHR steroid hormone signaling pathways are required for the daf-16/FOXO arrest-defective phenotype, suggesting that daf-16/FOXO represses dbl-1/TGF-β and daf-36. The dbl-1/TGF-β and daf-12/NHR pathways have not previously been shown to affect L1 development, but we found that disruption of these pathways delayed L1 development in fed larvae, consistent with these pathways promoting development in starved daf-16/FOXO mutants. Though the dbl-1/TGF-β and daf-12/NHR pathways are epistatic to daf-16/FOXO for the arrest-defective phenotype, disruption of these pathways does not suppress starvation sensitivity of daf-16/FOXO mutants. This observation uncouples starvation survival from developmental arrest, indicating that DAF-16/FOXO targets distinct effectors for each phenotype, and revealing that inappropriate development during starvation does not cause the early demise of daf-16/FOXO mutants. Overall, this study shows that daf-16/FOXO promotes developmental arrest cell-nonautonomously by repressing pathways that promote larval development.
2016-05-27 | GSE69329 | GEO