Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11425020_1.fastq.gz | Fastqsanger.gz | |||
| SRR11425020_2.fastq.gz | Fastqsanger.gz | |||
| SRR11425021_1.fastq.gz | Fastqsanger.gz | |||
| SRR11425021_2.fastq.gz | Fastqsanger.gz | |||
| SRR11425022_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 8 |
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Project description:Comparison of methylome of HEK293-CT cells and HEK293 cells stably over-expressing the BAHD1 gene (HEK-BAHD1) We used BS-seq to identify genomic regions differentially methylated upon overexpression of the chromatin repressor BAHD1 in HEK293 cells.
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Project description:Heatrich-BS was performed on 5 healthy volunteers and 15 CRC patient cell-free DNA. The Heatrich-BS predicted tumor fractions were compared with tumor burden values obtained by genomic methods such as targeted amplicon sequencing and low pass sequencing.
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Project description:<p>Wheat is a major staple crop grown across the globe. Fusarium crown rot (FCR) of wheat, caused by Fusarium pseudograminearum, is a destructive soil-borne disease that lacks effective sustainable control measures. Here, we assembled a cross-kingdom synthetic microbial community (SMC) comprising Trichoderma harzianum T19, Bacillus subtilis BS-Z15, and four other Bacillus strains, and evaluated its biocontrol efficacy against FCR under non-sterile soil conditions. The SMC treatment significantly suppressed FCR, reducing the disease severity index by approximately 70%. Wheat growth and yield were simultaneously enhanced: SMC inoculation nearly doubled plant biomass (with fresh and dry weights ~100% higher) and increased thousand-kernel weight by ~14% compared to the controls. In the rhizosphere, SMC improved soil health by elevating soil organic matter and nitrogen levels by over 50%, while mitigating pathogen-induced nutrient imbalances (excess available P and K) and boosting nutrient-cycling enzyme activities. Amplicon sequencing revealed that SMC suppressed pathogenic Fusarium in the rhizosphere and enriched beneficial microbes, including antagonistic fungi (Trichoderma, Chaetomium) and plant growth-promoting bacteria (Pseudomonas, Paenibacillus). Co-occurrence network analysis showed that SMC treatment restructured the rhizosphere microbial network with higher connectivity, stability, and a prevalence of positive cooperative interactions under F. pseudograminearum stress. Defense-related metabolites, such as epi-jasmonic acid, allantoin, Nβ-acetyltryptamine, and dihydrodaidzein, accumulated to higher levels with SMC, consistent with KEGG enrichment in pathways related to amino acid biosynthesis, carbon metabolism, signal transduction, and plant defense. These findings demonstrate that the cross-kingdom SMC modulates soil nutrients, microbial community structure, and rhizosphere metabolites to synergistically promote wheat growth and enhance resistance to FCR.</p>
2025-09-06 | MTBLS12946 | MetaboLights
Project description:whole-genome bisulfite sequencing (BS-seq) of HEK293 cells (HEK293-CT) and HEK293 cells stably over-expressing the BAHD1 gene (HEK-BAHD1)
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Project description:Bloom Syndrome (BS) is a recessive genetic disorder characterized by hyper-recombination and genome instability. It is caused by mutations in the conserved RecQ helicase gene, BLM, which is essential in maintaining genome integrity and unwinds various aberrant DNA structures. One such structure is DNA G-quadruplexes (G4s), which have broad regulatory functions. Although putative G4-forming sequences have been previously implicated in BS, it remains unclear what (dys)regulatory role, if any, endogenous G4 structures may play in BS. Here, we profiled chromatin accessibility and gene expression via ATAC-seq and RNA-seq and mapped endogenous G4 via ChIP-seq in wild-type (WT) vs. BS cell lines. We observed that in BS, differential G4 formation positively correlated with both chromatin accessibility and gene expression. Stabilizing G4 in WT cells with pyridostatin partially phenocopied BS. Additionally, data from a BS family showed that regions with increased chromatin accessibility in BS individuals were also enriched for G4-forming sequences. Our data showed that G4 formation is associated with higher chromatin accessibility and gene expression; likely in BS, unresolved G4 increases focal chromatin accessibility, thereby upregulating gene expression. In summary, our results revealed a central role of G4 in the molecular etiology of BS and provide a new perspective on BLM’s regulatory function through G4s.
2026-04-10 | GSE283480 | GEO
Project description:Bloom Syndrome (BS) is a recessive genetic disorder characterized by hyper-recombination and genome instability. It is caused by mutations in the conserved RecQ helicase gene, BLM, which is essential in maintaining genome integrity and unwinds various aberrant DNA structures. One such structure is DNA G-quadruplexes (G4s), which have broad regulatory functions. Although putative G4-forming sequences have been previously implicated in BS, it remains unclear what (dys)regulatory role, if any, endogenous G4 structures may play in BS. Here, we profiled chromatin accessibility and gene expression via ATAC-seq and RNA-seq and mapped endogenous G4 via ChIP-seq in wild-type (WT) vs. BS cell lines. We observed that in BS, differential G4 formation positively correlated with both chromatin accessibility and gene expression. Stabilizing G4 in WT cells with pyridostatin partially phenocopied BS. Additionally, data from a BS family showed that regions with increased chromatin accessibility in BS individuals were also enriched for G4-forming sequences. Our data showed that G4 formation is associated with higher chromatin accessibility and gene expression; likely in BS, unresolved G4 increases focal chromatin accessibility, thereby upregulating gene expression. In summary, our results revealed a central role of G4 in the molecular etiology of BS and provide a new perspective on BLM’s regulatory function through G4s.
2026-04-10 | GSE283477 | GEO
Project description:Bloom Syndrome (BS) is a recessive genetic disorder characterized by hyper-recombination and genome instability. It is caused by mutations in the conserved RecQ helicase gene, BLM, which is essential in maintaining genome integrity and unwinds various aberrant DNA structures. One such structure is DNA G-quadruplexes (G4s), which have broad regulatory functions. Although putative G4-forming sequences have been previously implicated in BS, it remains unclear what (dys)regulatory role, if any, endogenous G4 structures may play in BS. Here, we profiled chromatin accessibility and gene expression via ATAC-seq and RNA-seq and mapped endogenous G4 via ChIP-seq in wild-type (WT) vs. BS cell lines. We observed that in BS, differential G4 formation positively correlated with both chromatin accessibility and gene expression. Stabilizing G4 in WT cells with pyridostatin partially phenocopied BS. Additionally, data from a BS family showed that regions with increased chromatin accessibility in BS individuals were also enriched for G4-forming sequences. Our data showed that G4 formation is associated with higher chromatin accessibility and gene expression; likely in BS, unresolved G4 increases focal chromatin accessibility, thereby upregulating gene expression. In summary, our results revealed a central role of G4 in the molecular etiology of BS and provide a new perspective on BLM’s regulatory function through G4s.
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Project description:Pea root rot characterisation by amplicon sequencing
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Project description:We report the ChIP-seq of several histone modification markers for BS cells and H3K36me3 ChIP-seq for M cells, we found that BS-specific gene module trend to be regulated by histone acetylation.
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Project description:Proteomics analyses of 4T1 cells left untreated or treated with free BS, P-BS, or sequential P-BS-CM1→P-CM2
2024-03-07 | PXD050511 |