Cloeon viridulum
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA394104 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5822220_1.fastq.gz | Fastqsanger.gz | |||
| SRR5822220_2.fastq.gz | Fastqsanger.gz | |||
| SRR5822221_1.fastq.gz | Fastqsanger.gz | |||
| SRR5822221_2.fastq.gz | Fastqsanger.gz | |||
| SRR5822222_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 30 |
Similar Datasets
Project description:we used next-generation sequencing technology to characterize mRNA-seq of Cloeon viridulum (Ephemeroptera: Baetidae) among the young larva (YL), mature larva (ML), subimago (SI), imago (IM) stages, and mixture sampling (composite group, CG).
2018-06-01 | GSE101395 | GEO
Project description:Chronic inflammatory bowel disease (IBD) is associated with an increased risk of colorectal cancer (CRC) in historical cohorts. The pathways of oncogenesis of these CRCs, which are very different clinically from de novo CRCs, are currently unknown. The aim of our work is to identify specific molecular signatures of CRC occurring in the setting of IBD.
| 2390908 | ecrin-mdr-crc
Project description:Cloeon dipterum strain:GR | isolate:male_nymph Raw sequence reads
| PRJNA515246 | ENA
Project description:Cellular differentiation is orchestrated by lineage-specific transcription factors and associates with cell type-specific epigenetic signatures. Here, we utilized stage-specific, epigenetic "fingerprints" to deduce key transcriptional regulators of a cellular differentiation process. In the model of human macrophage differentiation, we globally mapped the distribution of epigenetic enhancer marks (histone H3 lysine 4 monomethylation, histone H3 lysine 27 acetylation, and the histone variant H2AZ) and show that cell type-specific epigenetic "fingerprints" correlate with specific, de novo derived motif signatures at all differentiation stages studied (hematopoietic progenitor cell, monocyte, macrophage). We validated the novel, de novo derived, macrophage-specific enhancer signature which included ETS, CEBP, bZIP, EGR, E-Box and NFkB motifs by ChIP-sequencing for a subset of motif corresponding transcription factors (PU.1, C/EBPbeta, and EGR2) which confirmed their predicted association with differentiation-associated epigenetic changes. This study highlights the power of genome-wide epigenetic profiling studies to reveal novel functional insights. It describes the dynamic enhancer landscape of human macrophage differentiation and provides a unique resource for macrophage biologists. ChIP-seq of 3 histone marks and 3 transcription factors in human blood monocytes and macrophages
2012-05-02 | E-GEOD-31621 | biostudies-arrayexpress
Project description:We combined multi-omics approaches including de novo transcriptome assembly, ribosome profiling and MS-based peptidomics to study the global role of mRNA translation and small ORFs (sORFs) in rice herbicide resistant mutant.
2021-05-11 | PXD025927 |
Project description:Aberrant expression of homeobox transcription factor HOXA9 is a central component of the leukemogenic program driven by diverse oncogenes. Here we show that HOXA9 overexpression in myeloid progenitor cells and pro-B cells leads to significant rearrangement of the epigenetic landscape with prominent emergence of cancer-specific de novo enhancers. HOXA9 acts as a pioneer factor at the de novo enhancers and is required for recruitment of transcription factor CEBP/ and the histone H3K4 methyltransferase MLL3/MLL4 complex. The HOXA9 function at de novo enhancers is distinct from its physiological role at enhancers during normal hematopoietic development. The MLL3/MLL4 complex physically interacts with HOXA9 and is required both for the active enhancer signatures at de novo enhancers and HOXA9/MEIS1-mediated leukemogenesis. The findings suggest that therapeutic targeting of HOXA9-dependent histone methylation could be an effective therapeutic strategy in acute leukemia associated with HOXA9 over expression.
2018-09-05 | GSE103446 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below. DNA methylation is an epigenetic modification associated with transcriptional repression of promoters and is essential for mammalian development. Establishment of DNA methylation is mediated by the de novo DNA methyltransferases DNMT3A and DNMT3B, whereas DNMT1 ensures maintenance of methylation through replication. Absence of these enzymes is lethal, and somatic mutations in these genes have been associated with several human diseases. How genomic DNA methylation patterns are regulated remains poorly understood, as the mechanisms that guide recruitment and activity of DNMTs in vivo are largely unknown. To gain insights into this matter we determined chromosomal binding and site-specific activity of the mammalian de novo DNA methyltransferases DNMT3A and DNMT3B. We show that both enzymes localize to methylated, CpG dense regions in mouse stem cells, yet are excluded from active promoters and enhancers. By specifically measuring sites of de novo methylation, we observe that enzymatic activity reflects chromosomal binding. De novo methylation increases with CpG density, yet is excluded from nucleosomes. Notably, we observed selective binding of DNMT3B to the bodies of transcribed genes, which leads to their preferential methylation. This targeting to transcribed sequences requires SETD2-mediated methylation of lysine 36 on histone H3 and a functional PWWP domain of DNMT3B. Together these findings reveal how sequence and chromatin cues guide de novo methyltransferase activity to ensure methylome integrity. Refer to individual Series
2015-01-22 | E-GEOD-57413 | biostudies-arrayexpress
Project description:DNA methylation is an epigenetic modification associated with transcriptional repression of promoters and is essential for mammalian development. Establishment of DNA methylation is mediated by the de novo DNA methyltransferases DNMT3A and DNMT3B, whereas DNMT1 ensures maintenance of methylation through replication. Absence of these enzymes is lethal, and somatic mutations in these genes have been associated with several human diseases. How genomic DNA methylation patterns are regulated remains poorly understood, as the mechanisms that guide recruitment and activity of DNMTs in vivo are largely unknown. To gain insights into this matter we determined chromosomal binding and site-specific activity of the mammalian de novo DNA methyltransferases DNMT3A and DNMT3B. We show that both enzymes localize to methylated, CpG dense regions in mouse stem cells, yet are excluded from active promoters and enhancers. By specifically measuring sites of de novo methylation, we observe that enzymatic activity reflects chromosomal binding. De novo methylation increases with CpG density, yet is excluded from nucleosomes. Notably, we observed selective binding of DNMT3B to the bodies of transcribed genes, which leads to their preferential methylation. This targeting to transcribed sequences requires SETD2-mediated methylation of lysine 36 on histone H3 and a functional PWWP domain of DNMT3B. Together these findings reveal how sequence and chromatin cues guide de novo methyltransferase activity to ensure methylome integrity. Whole-genome bisulfite sequencing for Dnmt1,3a,3b-triple-KO ES cells expressing DNMT3A2 or DNMT3B1 and for Dnmt1,3a,3b,Setd2-KO ES cells expressing DNMT3B1
2015-01-20 | E-GEOD-57411 | biostudies-arrayexpress