Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11565881_1.fastq.gz | Fastqsanger.gz | |||
| SRR11565881_2.fastq.gz | Fastqsanger.gz | |||
| SRR11565882_1.fastq.gz | Fastqsanger.gz | |||
| SRR11565882_2.fastq.gz | Fastqsanger.gz | |||
| SRR11565883_1.fastq.gz | Fastqsanger.gz |
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Project description:In this study, the carbohydrate composition of V. inaequalis tubular hyphae developed in and on the surface of CMs was characterized using a glycosidic linkage analysis, and the expression of cell wall enzymes analysed by RNA-seq and proteomics to shed light on the cell wall composition of this fungus during host-colonization.
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Project description:Gains and losses in DNA methylation are prominent genomic features of all mammalian cell types. To gain insight into mechanisms that could promote shifts in DNA 5-hydroxymethylation (5hmc) patterns and thus contribute to cell fate, including malignant transformation, we performed genome-wide mapping of 5hmc in purified wild type and Dnmt3a conditional knockout hematopoietic stem cells (HSCs) using cytosine-5-methylenesulphonate sequencing (CMS-seq). Comparing anti-CMS pulldown to input control, we identified 107,549 and 175,682 peaks of 5hmc enrichment in control and Dnmt3a knockout HSCs, respectively. Whole genome CMS-enriched bisulfite sequencing of secondarily-transplanted wild-type and Dnmt3a conditional knockout hematopoietic stem cells using Illumina HiSeq 2000
2014-01-22 | E-GEOD-53742 | biostudies-arrayexpress
Project description:We report the application of bioChIP-seq, bulk RNA-seq, Hi-C, and Massively parallel reporter assays (MPRAs) to characterize the p300-bound regulatory regions in murine cardiomyocytes (CMs). By obtaining ChIP-seq data of coactivator p300 from seven developmental stages of mouse CMs, we defined the dynamic p300 enhancers from embryonic CMs to adult CMs. We then validated the activity of dynamic p300 enhancers with AAV9-based MPRAs, we found dynamic p300 enhancers show dynamic activity from postnatal day 0 (P0) CMs to 4-week-old CMs. In addition, MRPA results suggest nuclear receptor motifs are required for the activity of some p300 late enhancers. With Hi-C data of E12.5, P0 and adult CMs, we identified chromatin structure changes such as chromatin loops, compartment switch, and new TAD boundaries are associated with dynamic p300 binding. This study provides data source of CM-selective p300 enhancers, chromatin 3D structure and gene expression during CM development and maturation.
2023-01-19 | GSE195901 | GEO
Project description:Maize LOB30 (Zm00001d036435) is a transcription factor and is specifically expressed in anthers. Our previous RNA-seq data showed that expression of some genes were upregualted in maize lob30 mutant maize anthers. To confirm these genes are the downstrem target genes, we generated proLOB30: GFP-LOB30 transgenic maize lines, collected stage 9 to stage10 anther materials and performed ChIP-seq using the GFP antibody.
2023-01-20 | GSE220176 | GEO
Project description:Small peptides (sPeptides), a class of biological molecules of less than 100 amio acids encoded by small open reading frames (sORFs), play important roles in multiple biological process. Here, we conducted a comprehensive study using mRNA-seq, Ribo-seq, and Mass Spectrometry (MS) on six tissues (each with at least two replicates) of maize, set up a bioinformatic pipeline, and performed a genome-wide scan of sORFs and sPeptides in maize. Our study sets up a guildline for the genome-wide scan of sORFs and sPeptides in plants by integrating Ribo-seq, and MS data, provides a more comprehensive resource of functional sPeptides in maize, and sheds light on the complex biological system of plants in a new perspective.
2021-05-30 | PXD025997 | Pride
Project description:Adenosine deaminases acting on RNA (Adar1 and Adar2) catalyze I-to-A RNA editing, a post-transcriptional mechanism involved in multiple cellular functions. The role of Adar1-dependent RNA editing in cardiomyocytes (CMs) remains unclear. Here we show that conditional deletion of Adar1 in CMs results in myocarditis progressively evolving into dilated cardiomyopathy and heart failure at only 6 months of age. Adar1 depletion drives activation of interferon signaling genes (ISGs) in the absence of apoptosis and cytokine activation, and reduces the hypertrophic response of CMs upon pressure overload. Interestingly, ablation of the cytosolic sensor MDA5 prevents cardiac ISG activation and delays disease onset, but does not rescue the long-term lethal phenotype elicited by conditional deletion of Adar1. Retention of a single catalytically inactive Adar1 allele in CMs, in combination with MDA5 depletion, however, completely restores the cardiac function and prevents heart failure. Finally, ablation of interferon regulatory factor 7 (Irf7) attenuates the phenotype of Adar1-deficient CMs to a similar extent as MDA5 depletion, highlighting Irf7 as the main regulator of the immune response triggered by lack of Adar1 in CMs.
2022-08-24 | PXD024974 | Pride
Project description:Purpose: LMNA-DCM accounts for 5-10% of DCM cases and has an age-related penetrance whose onset typically appears between the ages of 30 and 40. However, the precise mechanisms linking the LMNA mutation to increased arrhythmogenicity are still unknown. Methods: We utilized human iPSC-CMs RNA-seq, ChIP-seq, and ATAC-seq technologies. Results: The electrophysiological studies of iPSC-CMs identify the LMNA mutation as a cause of increased arrhythmogenicity in mutant iPSC-CMs through abnormal calcium homeostasis. We find that the mutations in LMNA disrupt the global chromatin conformation, resulting in hyper-activation of the platelet-derived growth factor (PDGF) signaling pathway in LMNA-mutant iPSC-CMs. Inhibition of the PDGF signaling pathway can rescue the arrhythmic phenotype of mutant iPSC-CMs. Conclusions: These findings were corroborated in cardiac tissues from healthy and LMNA-DCM patients, thus confirming a novel mechanism of LMNA-DCM pathogenesis both in vitro and in vivo.
2019-07-05 | GSE118884 | GEO
Project description:Purpose: LMNA-DCM accounts for 5-10% of DCM cases and has an age-related penetrance whose onset typically appears between the ages of 30 and 40. However, the precise mechanisms linking the LMNA mutation to increased arrhythmogenicity are still unknown. Methods: We utilized human iPSC-CMs RNA-seq, ChIP-seq, and ATAC-seq technologies. Results: The electrophysiological studies of iPSC-CMs identify the LMNA mutation as a cause of increased arrhythmogenicity in mutant iPSC-CMs through abnormal calcium homeostasis. We find that the mutations in LMNA disrupt the global chromatin conformation, resulting in hyper-activation of the platelet-derived growth factor (PDGF) signaling pathway in LMNA-mutant iPSC-CMs. Inhibition of the PDGF signaling pathway can rescue the arrhythmic phenotype of mutant iPSC-CMs. Conclusions: These findings were corroborated in cardiac tissues from healthy and LMNA-DCM patients, thus confirming a novel mechanism of LMNA-DCM pathogenesis both in vitro and in vivo.
2019-07-05 | GSE118883 | GEO