Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR23984832_1.fastq.gz | Fastqsanger.gz | |||
| SRR23984832_2.fastq.gz | Fastqsanger.gz | |||
| SRR23984833_1.fastq.gz | Fastqsanger.gz | |||
| SRR23984833_2.fastq.gz | Fastqsanger.gz | |||
| SRR23984834_1.fastq.gz | Fastqsanger.gz |
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Project description:In Xenopus, establishment of the anterior-posterior axis involves two key signalling pathways, canonical Wnt and Nodal-related TGF-β. There are also a number of transcription factors that feedback upon these pathways. The homeodomain protein Hex, an early marker of anterior positional information, acts as a transcriptional repressor suppressing induction and propagation of the Spemman organiser while specifying anterior identity. We show that Hex promotes anterior identity by amplifying the activity of canonical Wnt signalling. Hex exerts this activity by inhibiting the expression of Tle-4, a member of the Groucho family of transcriptional co-repressors that we identified as a Hex target in embryonic stem (ES) cells and Xenopus embryos. This Hex-mediated enhancement of Wnt signalling results in the up-regulation of the Nieuwkoop centre genes Siamois and Xnr-3 and the subsequent increased expression of the anterior endodermal marker Cerberus and other mesendodermal genes downstream of Wnt signalling. We also identified Nodal as a Hex target in ES cells. We demonstrate that in Xenopus, the Nodal-related genes Xnr-1 and 2, but not 5 and 6, are regulated directly by Hex. The identification of Nodal-related genes as Hex targets explains the ability of Hex to suppress induction and propagation of the organiser. Together these results support a model in which Hex acts early in development to reinforce a Wnt-mediated, Nieuwkoop-like signal to induce anterior endoderm, and later in this tissue to block further propagation of Nodal-related signals. The ability of Hex to regulate the same targets in both Xenopus and mouse implies this model is conserved. Keywords: genetic modification
2006-09-01 | GSE5141 | GEO
Project description:Hexadecenal, a trans (-2,3-) unsaturated fatty aldehyde, is an intermediate of the sphingolipid degradation pathway. This pathway, induced during cellular stress, involves the conversion of sphingosine-1-phosphate to hexadecenal by Sphingosine-1-Phosphate-Lyase (SPL) in humans and DPL1 in yeast. Hexadecenal is further metabolized to hexadecenoic acid by Fatty Aldehyde Dehydrogenase (ALDH3A2 in humans and HFD1 in yeast). Trans-2-hexadecenal (t-2-hex), has been found to induce mitochondrial dysfunction in a conserved manner from yeast to humans. However, the specific mechanisms and biological targets underlying this lipid-induced mitochondrial inhibition remain largely unknown. In this study, we employed unbiased transcriptomic approaches using the Saccharomyces cerevisiae yeast model to elucidate the principal mechanisms and biological targets associated with t-2-hex-induced mitochondrial dysfunction. To investigate the effects of t-2-hex, we utilized an hfd1 mutant strain lacking the HFD1 gene. This strain exhibited increased sensitivity to t-2-hex treatment compared to wild-type cells. Exponentially growing hfd1 mutant cells were exposed to 100 μM t-2-hex for a duration of 3 hours, while control cells were incubated with the solvent dimethyl sulfoxide (DMSO), in which hexadecenal is dissolved. Total RNA was extracted from both treated and control cells for high-throughput sequencing analysis. Through transcriptomic profiling, we aimed to identify differentially expressed genes, pathways, and regulatory networks associated with t-2-hex-induced mitochondrial dysfunction in yeast. This study provides a comprehensive analysis of the transcriptional response to t-2-hex treatment, shedding light on the molecular mechanisms and potential biological targets underlying lipid-induced mitochondrial dysfunction.
2023-07-31 | E-MTAB-13188 | biostudies-arrayexpress
Project description:In Xenopus, establishment of the anterior-posterior axis involves two key signalling pathways, canonical Wnt and Nodal-related TGF-β. There are also a number of transcription factors that feedback upon these pathways. The homeodomain protein Hex, an early marker of anterior positional information, acts as a transcriptional repressor suppressing induction and propagation of the Spemman organiser while specifying anterior identity. We show that Hex promotes anterior identity by amplifying the activity of canonical Wnt signalling. Hex exerts this activity by inhibiting the expression of Tle-4, a member of the Groucho family of transcriptional co-repressors that we identified as a Hex target in embryonic stem (ES) cells and Xenopus embryos. This Hex-mediated enhancement of Wnt signalling results in the up-regulation of the Nieuwkoop centre genes Siamois and Xnr-3 and the subsequent increased expression of the anterior endodermal marker Cerberus and other mesendodermal genes downstream of Wnt signalling. We also identified Nodal as a Hex target in ES cells. We demonstrate that in Xenopus, the Nodal-related genes Xnr-1 and 2, but not 5 and 6, are regulated directly by Hex. The identification of Nodal-related genes as Hex targets explains the ability of Hex to suppress induction and propagation of the organiser. Together these results support a model in which Hex acts early in development to reinforce a Wnt-mediated, Nieuwkoop-like signal to induce anterior endoderm, and later in this tissue to block further propagation of Nodal-related signals. The ability of Hex to regulate the same targets in both Xenopus and mouse implies this model is conserved. Experiment Overall Design: Identification of Hex target genes In Xenopus, the establishment of the anterior-posterior axis involves two key signalling pathways, the canonical Wnt and the Nodal-related TGF-β and a number of transcription factors that feedback upon these pathways. The homeodomain protein Hex, an early marker of anterior positional information, is a transcriptional repressor that suppresses the induction and propagation of the Spemman organiser while specifying anterior identity. Using microarray expression profiling we identified mouse Tle-4 as a Hex target in Embryonic Stem (ES) cells and showed that Tle-4 expression is directly regulated by Hex in Xenopus embryos. We also identified Nodal as a Hex target in ES cells. Taken together these results support a model in which Hex acts early in development to reinforce a Wnt-mediated, Nieuwkoop-like signal to induce anterior endoderm and later in this tissue to block further propagation of Nodal-related signals. The ability of Hex to regulate the same targets in both frog and mouse suggests that this model is conserved.
2008-06-13 | E-GEOD-5141 | biostudies-arrayexpress
Project description:IL22 induces antimicrobial peptides which influnce microbiota. We used 16s rRNA gene sequencing (16s DNA-seq) to analyze the microbiota with Fc or IL-22Fc treatment.
2024-08-01 | GSE242929 | GEO
Project description:Gene expression microarray exprement comparing differential expression between: 1) Early Diapause (ED), 2) Late Diapause (LD), 3) Non-Diapause (ND), 4) Hexane-induced diapause break (HEX). Four phenotypes (ED,ND,LD,HEX), four replicate pools of four individuals (four individuals in each replicate) in each phenotype, four competitve hybs comparing each phenotype to every other phenotype.
2010-05-20 | E-GEOD-20526 | biostudies-arrayexpress
Project description:We have engineered the chromatin-modifying apparatus and formulated a novel technology, termed Clickable Chromatin Enrichment with parallel DNA sequencing (CliEn-seq), to probe genome-wide chromatin modification within living cells. Examine (E)-hex-2-en-5-ynylation mediated by engineered G9a Y1154A and GLP1 Y1211A in HEK293T cells.
2013-03-04 | E-GEOD-42792 | biostudies-arrayexpress
Project description:Lipid intermediates derived from sphingolipid metabolism are crucial regulators of mitochondrial function from yeast to humans. Among these intermediates, trans-2-hexadecenal (t-2hex) within the sphingolipid degradation pathway exhibits remarkable efficiency in inducing mitochondria-mediated cell death. In yeast cell cultures, the addition of t-2-hex triggers complete disintegration of the mitochondrial network, leading to subsequent cell death. This effect is particularly pronounced in yeast cells lacking the activity of the t-2-hex degrading enzyme, Hfd1. However, the molecular mechanisms of t-2-hex induction of mitochondrial dysfunction are completely unknown. In this project, we want to exploit the unprecedented power of yeast genetics to unveil novel genetic determinants involved in t-2-hex's pro-apoptotic function. To accomplish this, we employed the SATAY method, which combines saturated transposon mutagenesis with high-throughput sequencing to functionally explore the yeast genome. In our screening approach, hfd1 mutant cells harboring a plasmid-encoded inducible MiniDs transposon were induced by galactose, resulting in extensive integration of the transposon throughout the yeast genome. Cells with the plasmid excised and the transposon genomically integrated were pooled together, creating a high-density transposon library comprising approximately 2.3E+06 independent insertion mutants. Subsequently, the pooled mutant library was subjected to treatment with the mitochondria-mediated death inducer, t-2-hexadecenal. As a control, cells were also incubated with the solvent dimethyl sulfoxide (DMSO), in which hexadecenal is dissolved. Following the treatments, cells were collected for genomic DNA extraction and digestion, using restriction enzymes with frequent four-base pair recognition sites. The resulting library fragments were circularized using T4 DNA ligase, and the transposon-genome junctions were selectively amplified through PCR with outward-facing primers specific to the transposon. Finally, the pooled and purified amplicons were subjected to massive sequencing on an Illumina MiSeq platform. The obtained sequences were then aligned to the reference genome of Saccharomyces cerevisiae, allowing for the mapping of transposon insertions and the calculation of transposon counts per gene. This project enabled the identification of genes required for the resistance and toxicity to t-2hex.
2023-08-31 | E-MTAB-13208 | biostudies-arrayexpress
Project description:Gene expression microarray exprement comparing differential expression between: 1) Early Diapause (ED), 2) Late Diapause (LD), 3) Non-Diapause (ND), 4) Hexane-induced diapause break (HEX).
2010-05-20 | GSE20526 | GEO
Project description:The impact of mono-chronic S. stercoralis infection on the gut microbiome and microbial activities in infected participants was explored. The 16S rRNA gene sequencing of a longitudinal study with 2 sets of human fecal was investigated. Set A, 42 samples were matched, and divided equally into positive (Pos) and negative (Neg) for S. stercoralis diagnoses. Set B, 20 samples of the same participant in before (Ss+PreT) and after (Ss+PostT) treatment was subjected for 16S rRNA sequences and LC-MS/MS to explore the effect of anti-helminthic treatment on microbiome proteomes.
2023-11-07 | PXD037975 | JPOST Repository
Project description:We report that ES cells cultured in ground state (2i and 2i/LIF) culture conditions are heterogeneous and show heterogeneus expression of extraembryonic markers. Using a highly sensitive reporter for the endoderm marker Hex we can sort Hex high and low populations from either serum/LIF or 2i/LIF and demonstrate that they have different functional properties. Here we explored the transcriptional basis of these functional differences and noted that Hex low (HV-) and Hex high (HV+) populations showed more distinct expression profiles in 2i/LIF than in serum/LIF. Additionally in 2i/LIF the HV+ population showed an upregulation of extraembryonic markers (such as trophoblast stem cell specific genes) and also imprinted genes compared to the HV- population, which is not observed when these populations are sorted from serum/LIF. We also analysed the transcriptional effect of LIF in 2i by analysing unsorted ES cells cultured in either 2i alone or 2i with LIF. We observed that the addition of LIF led to an upregulation of extraembryonic markers but did not effect the expression of pluripotency genes, other than Klf4. Additionally, the most significantly upregulated genes from 2i/LIF cultured ES cells compared to 2i cultured ES cells showed the greatest correlation to placental tissue when compared to the GNF tissue specific expression database. This analysis, alongside functional experiments, suggested that HV+ ES cells in 2i/LIF corresponded to an extraembryonically primed population of cells and that the addition of LIF supported this population. RNA-seq of sorted Hex low and high expressing ES cell populations cultured in serum/LIF or 2i/LIF as well as unsorted ES cells from 2i or 2i/LIF.
2013-06-11 | E-GEOD-45182 | biostudies-arrayexpress