20 results for chip-seq drosophila
Maintenance of spatial gene expression by Polycomb-mediated repression after formation of a vertebrate body plan
Contributors: Rougeot, Julien, Chrispijn, Naomi D., Aben, Marco, Elurbe, Dei M., Andralojc, Karolina M., Murphy, Patrick J., Jansen, Pascal WTC, Vermeulen, Michiel, Cairns, Bradley R., Kamminga, Leonie M.
ChIP-seq: lane1_MPZezh2WT-24hpf-Ezh2__R.fastq.gz: 1 sample of ...ChIP-seq data from 24hpf wild-type (TU/TL background) whole embryo lysates...ChIP-seq data (with Drosophila H2Ay spike in) from 24hpf wild-type (TU ... This dataset contains zebrafish (Danio rerio) raw RNA and ChIP sequencing data: RNA-seq: RNAseq_Wildtype_rep.fastq.gz: 2 biological replicates of single-end RNA-seq data from 24hpf wild-type (TU/TL background) whole embryo lysates RNAseq_Wildtype_rep[3-6].fastq.gz 4 biological replicates of paired-end RNA-seq data from 24hpf wild-type (TU/TL background) whole embryo lysates ChIP-seq: lane1_MPZezh2WT-24hpf-Ezh2__R.fastq.gz: 1 sample of paired-end Ezh2 ChIP-seq data from 24hpf wild-type (TU/TL background) whole embryo lysates lane1_MPZezh2WT-24hpf-Rnf2__R.fastq.gz: 1 sample of paired-end Rnf2 ChIP-seq data from 24hpf wild-type (TU/TL background) whole embryo lysates lane1_MPZezh2WT-24hpf-H3K27me3__R.fastq.gz: 1 sample of paired-end H3K27me3 ChIP-seq data from 24hpf wild-type (TU/TL background) whole embryo lysates *MPZezh2WT-24hpf-H3K4me3*: 2 biological replicates of paired-end H3K4me3 ChIP-seq data from 24hpf wild-type (TU/TL background) whole embryo lysates MPZezh2WT-24hpf-Ezh2-spikein-13277_R.fastq.gz: 1 sample of paired-end Ezh2 ChIP-seq data (with Drosophila H2Ay spike in) from 24hpf wild-type (TU/TL background) whole embryo lysates MPZezh2WT-24hpf-H3K27A[cC]*: 2 biological replicates of paired-end H3K27ac ChIP-seq data from 24hpf wild-type (TU/TL background) whole embryo lysates MPZezh2WT-24hpf-H3K27me3-spikein-13275_R.fastq.gz: 1 sample of paired-end H3K27me3 ChIP-seq data (with Drosophila H2Ay spike in) from 24hpf wild-type (TU/TL background) whole embryo lysates
Contributors: Rich Jones
... Refine.bio survey list generator required CSV, tediously exported manually from GEO web interface. Ex: $ head accessions/Illumina\ HiSeq\ 2000.csv "Experiment Accession","Experiment Title","Organism Name","Instrument","Submitter","Study Accession","Study Title","Sample Accession","Sample Title","Total Size, Mb","Total RUNs","Total Spots","Total Bases","Library Name","Library Strategy","Library Source","Library Selection" "SRX4195895","4","Homo sapiens","Illumina HiSeq 2000","Kolling Institute, The University of Sydney","SRP150290","RET-altered microRNAs in MTC","SRS3406604","","370.5","1","15916120","795806000","4","miRNA-Seq","TRANSCRIPTOMIC","unspecified" "SRX4195894","3","Homo sapiens","Illumina HiSeq 2000","Kolling Institute, The University of Sydney","SRP150290","RET-altered microRNAs in MTC","SRS3406603","","362.43","1","16021366","801068300","3","miRNA-Seq","TRANSCRIPTOMIC","unspecified" "SRX4195893","6","Homo sapiens","Illumina HiSeq 2000","Kolling Institute, The University of Sydney","SRP150290","RET-altered microRNAs in MTC","SRS3406602","","407.58","1","18432342","921617100","6","miRNA-Seq","TRANSCRIPTOMIC","unspecified" "SRX4195892","5","Homo sapiens","Illumina HiSeq 2000","Kolling Institute, The University of Sydney","SRP150290","RET-altered microRNAs in MTC","SRS3406605","","347.33","1","16162471","808123550","5","miRNA-Seq","TRANSCRIPTOMIC","unspecified"
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Contributors: Duffy, David J., Krstic, Aleksandar, Halasz, Melinda, Schwarzl, Thomas, Konietzny, Anja, Iljin, Kristiina, Higgins, Desmond G., Kolch, Walter
ChIP-seq) ... Background: Retinoid therapy is widely employed in clinical oncology to differentiate malignant cells into their more benign counterparts. However, certain high-risk cohorts, such as patients with MYCN-amplified neuroblastoma, are innately resistant to retinoid therapy. Therefore, we employed a precision medicine approach to globally profile the retinoid signalling response and to determine how an excess of cellular MYCN antagonises these signalling events to prevent differentiation and confer resistance. Methods: We applied RNA sequencing (RNA-seq) and interaction proteomics coupled with network-based systems level analysis to identify targetable vulnerabilities of MYCN-mediated retinoid resistance. We altered MYCN expression levels in a MYCN-inducible neuroblastoma cell line to facilitate or block retinoic acid (RA)-mediated neuronal differentiation. The relevance of differentially expressed genes and transcriptional regulators for neuroblastoma outcome were then confirmed using existing patient microarray datasets. Results: We determined the signalling networks through which RA mediates neuroblastoma differentiation and the inhibitory perturbations to these networks upon MYCN overexpression. We revealed opposing regulation of RA and MYCN on a number of differentiation-relevant genes, including LMO4, CYP26A1, ASCL1, RET, FZD7 and DKK1. Furthermore, we revealed a broad network of transcriptional regulators involved in regulating retinoid responsiveness, such as Neurotrophin, PI3K, Wnt and MAPK, and epigenetic signalling. Of these regulators, we functionally confirmed that MYCN-driven inhibition of transforming growth factor beta (TGF-β) signalling is a vulnerable node of the MYCN network and that multiple levels of cross-talk exist between MYCN and TGF-β. Co-targeting of the retinoic acid and TGF-β pathways, through RA and kartogenin (KGN; a TGF-β signalling activating small molecule) combination treatment, induced the loss of viability of MYCN-amplified retinoid-resistant neuroblastoma cells. Conclusions: Our approach provides a powerful precision oncology tool for identifying the driving signalling networks for malignancies not primarily driven by somatic mutations, such as paediatric cancers. By applying global omics approaches to the signalling networks regulating neuroblastoma differentiation and stemness, we have determined the pathways involved in the MYCN-mediated retinoid resistance, with TGF-β signalling being a key regulator. These findings revealed a number of combination treatments likely to improve clinical response to retinoid therapy, including co-treatment with retinoids and KGN, which may prove valuable in the treatment of high-risk MYCN-amplified neuroblastoma.
Contributors: Maeda, Robert K., Karch, François
Drosophila third chromosome, the locus became known of as the bithorax...Drosophila ... After nearly 30 years of effort, Ed Lewis published his 1978 landmark paper in which he described the analysis of a series of mutations that affect the identity of the segments that form along the anterior-posterior (AP) axis of the fly (Lewis 1978). The mutations behaved in a non-canonical fashion in complementation tests, forming what Ed Lewis called a "pseudo-allelic" series. Because of this, he never thought that the mutations represented segment-specific genes. As all of these mutations were grouped to a particular area of the Drosophila third chromosome, the locus became known of as the bithorax complex (BX-C). One of the key findings of Lewis' article was that it revealed for the first time, to a wide scientific audience, that there was a remarkable correlation between the order of the segment-specific mutations along the chromosome and the order of the segments they affected along the AP axis. In Ed Lewis' eyes, the mutants he discovered affected "segment-specific functions" that were sequentially activated along the chromosome as one moves from anterior to posterior along the body axis (the colinearity concept now cited in elementary biology textbooks). The nature of the "segment-specific functions" started to become clear when the BX-C was cloned through the pioneering chromosomal walk initiated in the mid 1980s by the Hogness and Bender laboratories (Bender et al. 1983a; Karch et al. 1985). Through this molecular biology effort, and along with genetic characterizations performed by Gines Morata's group in Madrid (Sanchez-Herrero et al. 1985) and Robert Whittle's in Sussex (Tiong et al. 1985), it soon became clear that the whole BX-C encoded only three protein-coding genes (Ubx, abd-A, and Abd-B). Later, immunostaining against the Ubx protein hinted that the segment-specific functions could, in fact, be cis-regulatory elements regulating the expression of the three protein-coding genes. In 1987, Peifer, Karch, and Bender proposed a comprehensive model of the functioning of the BX-C, in which the "segment-specific functions" appear as segment-specific enhancers regulating, Ubx, abd-A, or Abd-B (Peifer et al. 1987). Key to their model was that the segmental address of these enhancers was not an inherent ability of the enhancers themselves, but was determined by the chromosomal location in which they lay. In their view, the sequential activation of the segment-specific functions resulted from the sequential opening of chromatin domains along the chromosome as one moves from anterior to posterior. This model soon became known of as the open for business model. While the open for business model is quite easy to visualize at a conceptual level, molecular evidence to validate this model has been missing for almost 30 years. The recent publication describing the outstanding, joint effort from the Bender and Kingston laboratories now provides the missing proof to support this model (Bowman et al. 2014). The purpose of this article is to review the open for business model and take the reader through the genetic arguments that led to its elaboration.
Contributors: Leung, Wilson, Marenco, Remi, Liu, Yating, Goecks, Jeremy, Elgin, Sarah C.R.
... G-OnRamp poster for the 2016 BD2K All Hands Meeting
Contributors: Deplancke, Bart
... This presentation was part of Day 5 of the Open Science in Practice Summer School #osip2017. Additional information can be found on osip2017.epfl.ch.
Unique cistrome defined as CsMBE is strictly required for Nrf2-sMaf heterodimer function in cytoprotection
Contributors: Otsuki, Akihito, Suzuki, Mikiko, Katsuoka, Fumiki, Tsuchida, Kouhei, Suda, Hiromi, Morita, Masanobu, Shimizu, Ritsuko, Yamamoto, Masayuki
... Nrf2-small Maf (sMaf) heterodimer is essential for the inducible expression of cytoprotective genes upon exposure to oxidative and xenobiotic stresses. While the Nrf2-sMaf heterodimer recognizes DNA sequences referred to as the antioxidant/electrophile responsive element (ARE/EpRE), we here define these DNA sequences collectively as CNC-sMaf binding element (CsMBE). In contrast, large and small Maf proteins are able to form homodimers that recognize the Maf recognition element (MARE). CsMBE and MARE share a conserved core sequence but they differ in the 5'-adjacent nucleotide neighboring the core. Because of the high similarity between the CsMBE and MARE sequences, it has been unclear how many target binding sites and target genes are shared by the Nrf2-sMaf heterodimers and Maf homodimers. To address this issue, we introduced a substitution mutation of alanine to tyrosine at position 502 in Nrf2, which rendered the DNA-binding domain structure of Nrf2 similar to Maf, and generated knock-in mice expressing the Nrf2(A502Y) mutant. Our chromatin immunoprecipitation-sequencing analyses showed that binding sites of Nrf2(A502Y)-sMaf were dramatically changed from CsMBE to MARE in vivo. Intriguingly, however, one-quarter of the Nrf2(A502Y)-sMaf binding sites also bound Nrf2-sMaf commonly and vice versa. RNA-sequencing analyses revealed that Nrf2(A502Y)-sMaf failed to induce expression of major cytoprotective genes upon stress stimulation, which increased the sensitivity of Nrf2(A502Y) mutant mice to acute acetaminophen toxicity. These results demonstrate that the unique cistrome defined as CsMBE is strictly required for the Nrf2-sMaf heterodimer function in cytoprotection and that the roles played by CsMBE differ sharply from those of MARE.
Contributors: Moretti, Charlotte, Vaiman, Daniel, Tores, Frederic, Cocquet, Julie
ChIP-Seq datasets performed on mouse round spermatids and four RNA-seq ... Background: During meiosis, the X and Y chromosomes are transcriptionally silenced. The persistence of repressive chromatin marks on the sex chromatin after meiosis initially led to the assumption that XY gene silencing persists to some extent in spermatids. Considering the many reports of XY-linked genes expressed and needed in the post-meiotic phase of mouse spermatogenesis, it is still unclear whether or not the mouse sex chromatin is a repressive or permissive environment, after meiosis. Results: To determine the transcriptional and chromatin state of the sex chromosomes after meiosis, we re-analyzed ten ChIP-Seq datasets performed on mouse round spermatids and four RNA-seq datasets from male germ cells purified at different stages of spermatogenesis. For this, we used the last version of the genome (mm10/GRCm38) and included reads that map to several genomic locations in order to properly interpret the high proportion of sex chromosome-encoded multicopy genes. Our study shows that coverage of active epigenetic marks H3K4me3 and Kcr is similar on the sex chromosomes and on autosomes. The post-meiotic sex chromatin nevertheless differs from autosomal chromatin in its enrichment in H3K9me3 and its depletion in H3K27me3 and H4 acetylation. We also identified a posttranslational modification, H3K27ac, which specifically accumulates on the Y chromosome. In parallel, we found that the X and Y chromosomes are enriched in genes expressed post-meiotically and display a higher proportion of spermatid-specific genes compared to autosomes. Finally, we observed that portions of chromosome 14 and of the sex chromosomes share specific features, such as enrichment in H3K9me3 and the presence of multicopy genes that are specifically expressed in round spermatids, suggesting that parts of chromosome 14 are under the same evolutionary constraints than the sex chromosomes. Conclusions: Based on our expression and epigenomic studies, we conclude that, after meiosis, the mouse sex chromosomes are no longer silenced but are nevertheless regulated differently than autosomes and accumulate different chromatin marks. We propose that post-meiotic selective constraints are at the basis of the enrichment of spermatid-specific genes and of the peculiar chromatin composition of the sex chromosomes and of parts of chromosome 14.
Contributors: Conesa, Ana, Madrigal, Pedro, Tarazona, Sonia, Gomez-Cabrero, David, Cervera, Alejandra, McPherson, Andrew, Szcześniak, Michał Wojciech, Gaffney, Daniel J., Elo, Laura L., Zhang, Xuegong
... RNA-sequencing (RNA-seq) has a wide variety of applications, but no single analysis pipeline can be used in all cases. We review all of the major steps in RNA-seq data analysis, including experimental design, quality control, read alignment, quantification of gene and transcript levels, visualization, differential gene expression, alternative splicing, functional analysis, gene fusion detection and eQTL mapping. We highlight the challenges associated with each step. We discuss the analysis of small RNAs and the integration of RNA-seq with other functional genomics techniques. Finally, we discuss the outlook for novel technologies that are changing the state of the art in transcriptomics.
Contributors: Menietti, Elena, Xu, Xiaoying, Ostano, Paola, Joseph, Jean-Marc, Lefort, Karine, Dotto, G Paolo
... CSL is a key transcriptional repressor and mediator of Notch signaling. Despite wide interest in CSL, mechanisms responsible for its own regulation are little studied. CSL down-modulation in human dermal fibroblasts (HDFs) leads to conversion into cancer associated fibroblasts (CAF), promoting keratinocyte tumors. We show here that CSL transcript levels differ among HDF strains from different individuals, with negative correlation with genes involved in DNA damage/repair. CSL expression is negatively regulated by stress/DNA damage caused by UVA, Reactive Oxygen Species (ROS), smoke extract, and doxorubicin treatment. P53, a key effector of the DNA damage response, negatively controls CSL gene transcription, through suppression of CSL promoter activity and, indirectly, by increased p21 expression. CSL was previously shown to bind p53 suppressing its activity. The present findings indicate that p53, in turn, decreases CSL expression, which can serve to enhance p53 activity in acute DNA damage response of cells.