Formaldehyde-crosslinking and immunoprecipitation (FA-CLIP) sequencing to identify ECT2 targets in Arabidopsis
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ABSTRACT:
PROVIDER: PRJNA422491 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6377850.fastq.gz | Fastqsanger.gz | |||
| SRR6377841_1.fastq.gz | Fastqsanger.gz | |||
| SRR6377841_2.fastq.gz | Fastqsanger.gz | |||
| SRR6377842_1.fastq.gz | Fastqsanger.gz | |||
| SRR6377842_2.fastq.gz | Fastqsanger.gz |
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Project description:Developed an efficient method to identify RNA binding sites for RNA-binding proteins in plants.
2018-06-21 | GSE108117 | GEO
Project description:RNA-seq and FA-CLIP studying ECT2 function in Arabidopsis
| PRJNA422488 | ENA
Project description:Abstract of associated menuscript; Quinones and alpha,beta-unsaturated carbonyls are naturally occurring electrophiles that target cysteine residues via thiol-(S)-alkylation. We analyzed the global expression profile of Bacillus subtilis to the toxic carbonyls methylglyoxal (MG) and formaldehyde (FA). Both carbonyl compounds cause a stress response characteristic for thiol-reactive electrophiles as revealed by the induction of the Spx, CtsR, CymR, PerR, ArsR, CzrA, CsoR and SigmaD regulons. MG and FA triggered also a SOS response which indicates DNA damage. Protection against FA is mediated by both the hxlAB operon, encoding the ribulose monophosphate pathway for FA fixation, and a thiol-dependent formaldehyde dehydrogenase (AdhA) and DJ-1/PfpI-family cysteine proteinase (YraA). The adhA-yraA operon and the yraC gene, encoding gamma-carboxymuconolactone decarboxylase, are positively regulated by the MerR-family regulator, YraB(AdhR). AdhR binds specifically to its target promoters which contain a 7-4-7 inverted repeat (CTTAAAG-N4-CTTTAAG) between the -35 and -10 elements. Activation of adhA-yraA transcription by AdhR requires the conserved Cys52 residue in vivo. We speculate that AdhR is redox-regulated via thiol-(S)-alkylation by aldehydes and that AdhA and YraA are specifically involved in reduction of aldehydes and degradation or repair of damaged thiol-containing proteins, respectively.
2008-12-13 | GSE13925 | GEO
Project description:Abstract of associated menuscript; Quinones and alpha,beta-unsaturated carbonyls are naturally occurring electrophiles that target cysteine residues via thiol-(S)-alkylation. We analyzed the global expression profile of Bacillus subtilis to the toxic carbonyls methylglyoxal (MG) and formaldehyde (FA). Both carbonyl compounds cause a stress response characteristic for thiol-reactive electrophiles as revealed by the induction of the Spx, CtsR, CymR, PerR, ArsR, CzrA, CsoR and SigmaD regulons. MG and FA triggered also a SOS response which indicates DNA damage. Protection against FA is mediated by both the hxlAB operon, encoding the ribulose monophosphate pathway for FA fixation, and a thiol-dependent formaldehyde dehydrogenase (AdhA) and DJ-1/PfpI-family cysteine proteinase (YraA). The adhA-yraA operon and the yraC gene, encoding gamma-carboxymuconolactone decarboxylase, are positively regulated by the MerR-family regulator, YraB(AdhR). AdhR binds specifically to its target promoters which contain a 7-4-7 inverted repeat (CTTAAAG-N4-CTTTAAG) between the -35 and -10 elements. Activation of adhA-yraA transcription by AdhR requires the conserved Cys52 residue in vivo. We speculate that AdhR is redox-regulated via thiol-(S)-alkylation by aldehydes and that AdhA and YraA are specifically involved in reduction of aldehydes and degradation or repair of damaged thiol-containing proteins, respectively. WT (-FA) vs. WT (+ 1 mM FA), WT (-MG) vs. WT (+ 2.8 mM MG), WT (-MG) vs. WT (+ 5.6 mM MG). Each experiement was conducted triplicates using three independent total RNA preparations. For all datasets used for final analysis, untreated samples were labeled with Cy3 and treated samples with Cy5.
2010-05-15 | E-GEOD-13925 | biostudies-arrayexpress
Project description:Neurotoxicity of formaldehyde (FA) in the human health attracted intensive studies Long-term exposure to FA leads to learning and memory decline and is responsible for the multiple chemical sensitivity (MCS) or sick building syndrome (SBS). It was cleared that Formaldehyde impairs Learning and Memory in Hippocampal. however ,it is unclear if FA can disturb the olfactory bulb function miRNAs alterations were related to environmental chemical exposure. It was reported that FA inhale altered miRNAs expression in the nasal Epithelium and lung cells. In the present study, FA inhalation significatly alters miRNA expression profiles within olfactory bulb
2015-08-04 | GSE59369 | GEO
Project description:Formaldehyde (FA) is a commercially important chemical with numerous and diverse uses. In this study, a functional toxicogenomics approach was utilized in the model eukaryotic yeast Saccharomyces cerevisiae to identify genes and cellular processes modulating the cellular toxicity of FA. Our results demonstrate mutant strains deficient in multiple DNA repair pathways were sensitive to FA. The SKI complex and its associated factors, which regulate mRNA degradation by the exosome, were also required for FA tolerance..
2016-11-09 | GSE83398 | GEO
Project description:Neurotoxicity of formaldehyde (FA) in the human health attracted intensive studies Long-term exposure to FA leads to learning and memory decline and is responsible for the multiple chemical sensitivity (MCS) or sick building syndrome (SBS). It was cleared that Formaldehyde impairs Learning and Memory in Hippocampal. however ,it is unclear if FA can disturb the olfactory bulb function miRNAs alterations were related to environmental chemical exposure. It was reported that FA inhale altered miRNAs expression in the nasal Epithelium and lung cells. In the present study, FA inhalation significatly alters miRNA expression profiles within olfactory bulb Eight week ICR male mouse. Mice were randomly assigned to three groups. The FA group exposed to 3ppm FA for six hours for consecutive 1 and 7days in a chamber which was described previously. The standard group was kept in same condition except the FA. After expose, both group mice were deeply anesthetized with isoflurane and decapitated. The OB was rapidly dissected
2015-08-04 | E-GEOD-59369 | biostudies-arrayexpress
Project description:The ability to capture protein: DNA interactions in a quantitative, high-resolution, and temporal manner in the cell context is crucial for elucidating the mechanisms underlying transcriptional regulation. Chromatin immunoprecipitation followed by sequencing (ChIP-seq) is a widely used technique that enables the study of histone modifications and genome-wide interactions of transcription factors and chromatin regulators. Although ChIP-seq generates a vast amount of information, crosslinking conditions need to be carefully evaluated to minimize the capture of non-specific interactions. In this study, we conduct an in-depth analysis to evaluate the impact of crosslinking conditions on ChIP-seq results for two NF-kB family members, RelA and c-Rel. We titrate two commonly used chemical crosslinkers, formaldehyde and DSG. We demonstrate that while raising the crosslinking concentrations increases the total number of binding sites and the strength of the binding signal, high crosslinking conditions lead to an abundance of interactions detected at locations that lack anticipated motifs or annotations to potential NF-kB target genes. Our findings emphasize the importance of a comprehensive evaluation of ChIP-seq results and a cautious evaluation of chemical crosslinking conditions. Moreover, we compare ChIP-seq to CUT&TAG, a newer technique that does not require crosslinking. This comparison revealed strongly overlapping genomic interactions between the two methods. However, both methods display evidence of a large number of non-specific signals that exhibit little overlap between the two methods.
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Project description:Formaldehyde (FA) is an environmental and occupational chemical carcinogen. Recent studies demonstrated that exogenous FA caused only a modest increase in DNA adducts above levels caused by endogenous FA. This raised a possibility that epigenetic mechanisms might contribute to FA-mediated carcinogenicity. Here we report a drastic decrease of acetylation of N-terminal tails of the cytosolic histones following FA exposure, the modifications important for histone nuclear import and assembly into chromatin. In fact, the amount of histone proteins in chromatin fraction decreases following FA exposure. Moreover, the histone depletions are evident at most of the genomic loci we tested, suggesting that FA compromises chromatin assembly. Notably, FA increases chromatin accessibility and changes expression of hundreds of cancer-related genes. Importantly, the knockdown of histone H3.3 (a H3 variant), which mimics inhibition of chromatin assembly, facilitates FA-mediated cell transformation. We propose that inhibiting chromatin assembly represents a novel mechanism for FA carcinogenesis.
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