Ontology highlight
ABSTRACT:
PROVIDER: PRJNA995587 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25303202_1.fastq.gz | Fastqsanger.gz | |||
| SRR25303202_2.fastq.gz | Fastqsanger.gz | |||
| SRR25303203_1.fastq.gz | Fastqsanger.gz | |||
| SRR25303203_2.fastq.gz | Fastqsanger.gz | |||
| SRR25303204_1.fastq.gz | Fastqsanger.gz |
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Project description:Cdc6-2 functions as a master regulator in mediating DNA damage response
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Project description:DNA methylation is an important regulator of genome function in the eukaryotes, but it is currently unclear if the same is true in prokaryotes. While regulatory functions have been demonstrated for a small number of bacteria, there have been no large-scale studies of prokaryotic methylomes and the full repertoire of targets and biological functions of DNA methylation remains unclear. Here we applied single-molecule, real-time sequencing to directly study the methylomes of 232 phylogenetically diverse prokaryotes. Collectively, we identified 834 methylated motifs, enabling the specific annotation of 415 DNA methyltransferases (MTases), and adding substantially to existing databases of MTase specificities. While the majority of MTases function as components of restriction-modification systems, 139 MTases have no cognate restriction enzyme in the genome, suggesting some other functional role. Several of these âorphanâ MTases are conserved across species and exhibit patterns of DNA methylation consistent with known regulatory MTases. Based on these patterns of methylation, we identify candidate novel regulators of gene expression in several phyla of bacteria, and candidate regulators of DNA replication in Haloarchaea. Together these data substantially advance our knowledge of DNA restriction-modification systems, and hint at a wider role for methylation in prokaryotic genome regulation. Single-molecule, real-time sequencing of DNA modifications across 232 diverse prokaryotic genomes.
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Project description:The conserved TFIIH helicases XPB and XPD play key roles in transcription initiation and DNA repair. To investigate the functions of these helicases on a genome-wide scale, we performed ChIP-seq of endogenous XPB and XPD in the HT1080 human fibrosarcoma cell line. 2 ChIP samples and 1 unenriched input control from the same crosslinked chromatin pool
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Project description:Egr1 is a master regulator of regenerative senescence and cardiac repair
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Project description:The presence of oxidized DNA lesions, such as 7,8-dihydro-8-oxoguanine (8-oxoG) and apurinic/apyrimidinic sites (AP sites), has been described as epigenetic signals that are involved in gene expression control. In mammals, Apurinic-apyrimidinic endonuclease 1/Redox factor-1 (APE1/Ref-1) is the main AP endonuclease of the base excision repair (BER) pathway and is involved in active demethylation processes. In addition, APE1/Ref-1, through its redox function, regulates several transcriptional factors. However, the transcriptional control targets of each APE1 function are not completely known. In this study, a transcriptomic approach was used to investigate the effects of chemical inhibition of APE1/Ref-1 redox or DNA repair functions by E3330 or methoxyamine (MX) in an inflammatory cellular model. Under lipopolysaccharide (LPS) stimulation, both E3330 and MX reduced the expression of some cytokines and chemokines. Interestingly, E3330 treatment reduced cell viability after 48 h of the treatment. Genes related to inflammatory response and mitochondrial processes were downregulated in both treatments. In the E3330 treatment, RNA processing and ribosome biogenesis genes were downregulated, while they were upregulated in the MX treatment. Furthermore, in the E3330 treatment, the cellular stress response was the main upregulated process, while the cellular macromolecule metabolic process was observed in MX-upregulated genes. Nuclear respiratory factor 1 (NRF1) was predicted to be a master regulator of the downregulated genes in both treatments, while the ETS transcription factor ELK1 (ELK1) was predicted to be a master regulator only for E3330 treatment. Decreased expression of ELK1 and its target genes and a reduced 28S/18S ratio were observed, suggesting impaired rRNA processing. In addition, both redox and repair functions can affect the expression of NRF1 and GABPA target genes. The master regulators predicted for upregulated genes were YY1 and FLI1 for the E3330 and MX treatments, respectively. In summary, the chemical inhibition of APE1/Ref-1 affects gene expression regulated mainly by transcriptional factors of the ETS family, showing partial overlap of APE1 redox and DNA repair functions, suggesting that these activities are not entirely independent. This work provides a new perspective on the interaction between APE1 redox and DNA repair activity in inflammatory response modulation and transcription.
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Project description:Mutations in the tumour suppressor BRCA2 are associated with predisposition to breast and ovarian cancers. BRCA2 has a central role in genome integrity by facilitating the repair of toxic DNA double-strand breaks (DSBs) by homologous recombination. BRCA2 acts by promoting RAD51 nucleofilament formation on resected single-stranded DNA, but how BRCA2 activity is regulated during HR is not fully understood. Here, we delineate a pathway where ATM and ATR kinases phosphorylate a highly conserved region in BRCA2 in response to DNA DSBs. These phosphorylations stimulate the binding of the protein phosphatase PP2A-B56 to BRCA2 through a conserved binding motif. We show that the phosphorylation-dependent formation of the BRCA2-PP2A-B56 complex is required for efficient RAD51 loading to sites of DNA damage and HR-mediated DNA repair. Moreover, we find that several cancer-associated mutations in BRCA2 deregulate the BRCA2-PP2A-B56 interaction and sensitize cells to PARP inhibition. Collectively, our work uncovers PP2A-B56 as a positive regulator of BRCA2 function in HR with clinical implications for BRCA2 and PP2A-B56 mutated cancers.
2021-07-26 | MSV000087884 | MassIVE
Project description:Epigenetic remodeling is essential for oncogene-induced cellular transformation and malignancy. In contrast to histone posttranslational modification, how oncogenic signaling remodels DNA methylation remains poorly understood. The oncoprotein YAP, a coactivator of the TEAD transcription factors mediating Hippo signaling, is widely activated in human cancer. Here we identify the 5-methylcytosine dioxygenase TET1 as a direct YAP target and a master regulator that coordinates the genome-wide epigenetic and transcriptional reprogramming of YAP target genes in the liver. YAP activation induces the expression of TET1, which physically interacts with TEAD to cause regional DNA demethylation, histone H3K27 acetylation and chromatin opening in YAP target genes to facilitate transcriptional activation. Loss of TET1 not only reverses YAP-induced epigenetic and transcriptional changes but also suppresses YAP-induced hepatomegaly and tumorigenesis. These findings exemplify how oncogenic signaling regulates site specificity of DNA demethylation to promote tumorigenesis and implicate TET1 as a potential target for modulating YAP signaling in physiology and diseases.
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Project description:Lymphocytes represent basic components of vertebrate adaptive immune systems, suggesting the utility of non-mammalian models to define the molecular basis of their development and differentiation. Our forward genetic screens in zebrafish for recessive mutations affecting early T cell development revealed several major genetic pathways. The identification of lineage-specific transcription factors and specific components of cytokine signaling and DNA replication/repair pathways known from studies of immuno-compromised mammals provided an evolutionary cross-validation of the screen design. Unexpectedly, however, certain pre-mRNA processing factor genes, including tnpo3, encoding a regulator of alternative splicing, were also found to play a specific role in early T cell development. In both zebrafish and mouse, TNPO3 deficiency impairs intrathymic T cell differentiation, illustrating evolutionarily conserved and cell type-specific functions of certain pre-mRNA processing factor.
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Project description:The conserved TFIIH helicases XPB and XPD play key roles in transcription initiation and DNA repair. To investigate the functions of these helicases on a genome-wide scale, we performed ChIP-seq of endogenous XPB and XPD in the HT1080 human fibrosarcoma cell line.
2014-02-18 | GSE44849 | GEO