Ontology highlight
ABSTRACT:
PROVIDER: PRJNA698745 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13608000_1.fastq.gz | Fastqsanger.gz | |||
| SRR13608000_2.fastq.gz | Fastqsanger.gz | |||
| SRR13608001_1.fastq.gz | Fastqsanger.gz | |||
| SRR13608001_2.fastq.gz | Fastqsanger.gz | |||
| SRR13608002_1.fastq.gz | Fastqsanger.gz |
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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
Project description:Shot-gun whole cell lysate proteomics data from pure and enriched microbes were de-novo sequenced using PEAKS de Novo. The obtained peptide sequence lists serves as a test data for the peptide-centric taxonomy database Unipept.
2021-03-15 | PXD016992 | Pride
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. Genome-wide binding analysis for biotin-tagged DNMT3A2 and DNMT3B and variants in wild type ES, wild type neuroprogenitor cells, ES cells triple-KO for Dnmt1,3a,3b and ES cell mutant for Setd2
2015-01-20 | E-GEOD-57412 | biostudies-arrayexpress
Project description:In plants, maintenance-methylation mediated by METHYLTRANSFERASE-1 (MET1), siRNA-directed de-novo methylation, and chromatin remodeling by DECREASE IN DNA METHYLATION -1 (DDM1) promote transcriptional gene-silencing of transposable elements (TEs). This process is mostly investigated at steady states reflecting how long-established silent conditions are maintained, faithfully re-iterated or temporarily modified during growth, stress and over generations. How invasive TEs are detected and silenced de novo, however, remains largely unknown. Using inbred lineages of hybrid Arabidopsis epigenomes combining wild-type and met1 or ddm1 chromosomes, we have deciphered the timing, spatial distribution and mechanisms underpinning the proliferation and eventual demise of the endogenous retrotransposon évadé (EVD). Both developmental and molecular features of EVD biology, including a remarkable ability to evade RNA interference, ultimately contribute to its silencing over multiple generations. The underlying processes are accompanied by widespread diversification of the Arabidopsis genome and de-novo epiallelism creating an extensive reservoir of selectable and potentially adaptive traits.
2013-07-02 | GSE43412 | GEO
Project description:It has been reported that a number of small coding genes (30–100 amino acids) tend to be lineage-specifically emerged in evolution but such de-novo genes tend to be missed in genomes. Plant mitochondrial genomes might be fostering sources of de-novo genes because of a high rearrangement rate. However, the functional role of de-novo genes derived from mitochondria is unclear. Here, in the best model species of plants (Arabidopsis thaliana), we showed that Arabidopsis-specifically emerged de-novo genes derived from mitochondrial genome contributed to phenotypic variation in a species. We previously identified 49 candidates of small coding genes inducing abnormal morphological changes on overexpression in the nuclear genome. Among them, we focused on a candidate (sORF2146) potentially encoding 66 amino acids in large-scale intergenic genomic transferring region from mitochondrial genome. Comparative genome analysis showed that sORF2146 had been appeared in Arabidopsis lineage. Mitochondrial sORF2146 is fixed among A. thaliana ecotypes but nucleus sORF2146 is not fixed in A. thaliana ecotypes. After showing evidence that nucleus sORF2146 was transcribed and translated as a coding gene, we performed transcriptome analysis in transgenic plant overexpressing sORF2146. Genes associated with flowering transition are highly regulated in the transgenic plant. We then examined phenotypic effects of overexpression and knockdown transgenic plant. Overexpression and knockdown transgenic plant induce late and early flowering, respectively. Taken together, we conclude that a nucleus de-novo gene derived from mitochondria contributes to the variation of floral timing in Arabidopsis population.
2021-09-24 | GSE184689 | GEO
Project description:To test the hypothesis that the propensity for silencing of tumor suppressor genes in the respiratory epithelium of chronic smokers by promoter hypermethylation is influenced by sequence variations that modify the activity of genes and microRNAÕs that directly or indirectly influence de novo methylation and chromatin remodeling.
2014-09-29 | ST000104 | MetabolomicsWorkbench
Project description:The aberrant gain of DNA methylation at CpG islands (CGIs) is frequently observed in colorectal tumours and may silence the expression of tumour suppressors such as MLH1. Current models propose that these CGIs are targeted by de novo DNA methyltransferases (DNMTs) in a sequence-specific manner but this has not been tested. Using ectopically integrated CGIs, we find that aberrantly methylated CGIs are subject to low levels of de novo DNMT activity in colorectal cancer cells. By delineating DNMT targets, we find that instead de novo DNMT activity is targeted primarily to CGIs marked by the histone modification H3K36me3, a mark associated with transcriptional elongation. These H3K36me3 marked CGIs are heavily methylated in colorectal tumours and the normal colon suggesting that de novo DNMT activity at CGIs in colorectal cancer is focused on similar targets to normal tissues and not greatly remodelled by tumourigenesis.
2020-11-24 | GSE158405 | GEO
Project description:The aberrant gain of DNA methylation at CpG islands (CGIs) is frequently observed in colorectal tumours and may silence the expression of tumour suppressors such as MLH1. Current models propose that these CGIs are targeted by de novo DNA methyltransferases (DNMTs) in a sequence-specific manner but this has not been tested. Using ectopically integrated CGIs, we find that aberrantly methylated CGIs are subject to low levels of de novo DNMT activity in colorectal cancer cells. By delineating DNMT targets, we find that instead de novo DNMT activity is targeted primarily to CGIs marked by the histone modification H3K36me3, a mark associated with transcriptional elongation. These H3K36me3 marked CGIs are heavily methylated in colorectal tumours and the normal colon suggesting that de novo DNMT activity at CGIs in colorectal cancer is focused on similar targets to normal tissues and not greatly remodelled by tumourigenesis.
2020-11-24 | GSE158404 | GEO