Gene expression profiling of retinoic acid (RA)-treated embryoid bodies (EBs) derived from Elongin A+/+ and Elongin A-/- ES cells.
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Takashi yasukawa
PROVIDER: E-GEOD-30911 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:The ability of cells to perceive and translate versatile cues into differential chromatin and transcriptional states is critical for many biological processes1-4. In plants, timely transition to a flowering state is crucial for successful reproduction5-7. EARLY BOLTING IN SHORT DAY (EBS) is a negative transcriptional regulator that prevents premature flowering in Arabidopsis8,9. Here, we revealed that bivalent bromo-adjacent homology (BAH)-plant homeodomain (PHD) reader modules of EBS bind H3K27me3 and H3K4me3, respectively. A subset of EBS-associated genes was co-enriched with H3K4me3, H3K27me3, and the Polycomb repressor complex 2 (PRC2). Interestingly, EBS adopts an auto-inhibition mode to mediate its binding preference switch between H3K27me3 and H3K4me3. This binding balance is critical because disruption of either EBS-H3K27me3 or EBS-H3K4me3 interaction induces EBS-mediated early floral transition. This study identifies a single bivalent chromatin reader capable of recognizing two antagonistic histone marks and reveals a distinct mechanism of interplay between active and repressive chromatin states.The ability of cells to perceive and translate versatile cues into differential chromatin and transcriptional states is critical for many biological processes1-4. In plants, timely transition to a flowering state is crucial for successful reproduction5-7. EARLY BOLTING IN SHORT DAY (EBS) is a negative transcriptional regulator that prevents premature flowering in Arabidopsis8,9. Here, we revealed that bivalent bromo-adjacent homology (BAH)-plant homeodomain (PHD) reader modules of EBS bind H3K27me3 and H3K4me3, respectively. A subset of EBS-associated genes was co-enriched with H3K4me3, H3K27me3, and the Polycomb repressor complex 2 (PRC2). Interestingly, EBS adopts an auto-inhibition mode to mediate its binding preference switch between H3K27me3 and H3K4me3. This binding balance is critical because disruption of either EBS-H3K27me3 or EBS-H3K4me3 interaction induces EBS-mediated early floral transition. This study identifies a single bivalent chromatin reader capable of recognizing two antagonistic histone marks and reveals a distinct mechanism of interplay between active and repressive chromatin states.v
2019-09-09 | PXD009794 | Pride
Project description:Keratin cytoskeletal proteins are crucial for the maintenance of skin integrity. Mutations in genes coding for K5 and K14 cause the human skin disorder epidermolysis bullosa simplex (EBS) leading to substantial alterations in keratin assembly and collapse of keratin filaments into cytoplasmic protein aggregates. The phenotypic consequences of K5 and K14 mutations comprise fragility of basal keratinocytes and skin blistering upon mild mechanical trauma. Treatment of EBS is only supportive and consists primarily of wound care and avoidance of mechanical stress. Besides symptomatic care, no efficient therapeutic treatment is available for EBS. In the present study, we used patient-derived keratinocytes carrying the most frequent K14.R125C mutation as a reproducible EBS model to understand EBS pathomechanisms and to develop a therapy approach aimed to restore a functional keratin network. Numerous post-translational modifications (PTMs) such as phosphorylation have been reported to occur on keratins, which affect the organization of keratin networks. Whether keratin mutations affect the occurrence of PTMs and thereby keratin aggregation in EBS is yet unknown. We find that the K14.R125C mutation alters keratin and keratin-associated protein PTMs in distinct ways and suggest that disease mutations and altered PTMs aggravate keratin aggregation. We reason that chemical compounds affecting the interplay of mutations and PTMs enable the reformation of a keratin cytoskeleton from aggregates are potential candidates for combating EBS.
2022-06-29 | PXD030939 | Pride
Project description:These data include the genome wide location of different histone modifications by ChIP sequencing in mouse ES cells, and RNA Seq data generated from wild type and EED KO mouse ES cells and knocked down for unrelated protein and Setd2 protein. ChIP-Seq: Immuno-precipitation of formaldehyde cross-linked chromatin prepared from wild type mouse E14 ES cells, wild type E36 ES cells, EED KO E36 ES cells, wild type Embryoid bodies (Ebs), EED KO Embryoid bodies (Ebs EED KO) using specific antibody against different histone modifications. RNA-Seq: Total RNA extracted from wild type E36 ES cells, EED KO E36 ES cells, wild type E36 Embryoid bodies (Ebs), EED KO Embryoid bodies (Ebs EED KO), E14 Ctrl KD, E14 Setd2 KD.
2013-12-05 | E-GEOD-51006 | biostudies-arrayexpress
Project description:In this study, we profiled the change of gene expression by p53 knock-down on anaplastic thyroid carcinoma (ATC) cell line, KAT-18 cells using Applied Biosystem's Microarrays. When compared with the untreated control KAT-18 cells, 2,926 genes were found to have altered expression levels of 2-fold or more in cells treated with antisense p53 oligonucleotide. Microarray analysis revealed that p53 knock-down modified the expression of numerous apoptosis-related genes. Among those genes, 33 apoptosis pathway activators and 20 apoptosis pathway repressors were identified. We analyzed human thyroid carcinoma cell (KAT18) on Applied Biosystem Human 1700 Chip Arrays. There were control and test sample, respectively, KAT18 untreated and treated antisense p53.
2010-06-25 | E-GEOD-12912 | biostudies-arrayexpress
Project description:Pea3 and Erm are transcription factors belonging to the ETS family which are involved in tumorigenesis, particularly mammary oncogenesis. To elucidate the mechanism of Pea3/Erm induced tumorigenesis in mouse mammary cancerous MMT cells (ATCC CCL-51), we have down-regulated Pea3 or Erm expression in this cell line by using small interfering RNA and performed a microarray analysis using Applied Biosystems AB1700 technology to define target associated genes. Keywords: Comparative transcriptome hybridization, small interfering RNA, mouse mammary cancerous cells Mouse mammary cancerous MMT cells (ATCC CCL-51) have been transfected with a siRNA control, an erm-directed siRNA or an pea3-directed siRNA. MMT cells were also used to determine the modifications due to the transfection protocol. These conditions correspond to four sample. Two biological replicate were used for the MMT cells (control sample), three biological replicates were used for the siRNA control (control sample) and erm-directed siRNA (reference sample) MMT cells and four biological replicates were used for the pea3-directed siRNA (reference sample) MMT cells. Transcriptome profiles (28.218 validated mouse genes) were acquired using Applied Biosystems AB1700 technology, which make use of chemiluminescence-based detection chemistry.
2008-08-01 | E-GEOD-6588 | biostudies-arrayexpress
Project description:S6K1 Knockout mice has a lean phenotype and resitant to a High Fat Diet-induced obesity (Um S.H., Nature, 2004). Adipocyte differentiation consists of two step, first, commitment from stem cell to adipocyte progenitors and second, terminal differentiation from adipocyte progenitors to mature adipocyte. We studied S6K1-dependent gene expression regulation in early stage of commitment by employing ES cell(ESC)-Embryoid Bodies(EBs) differentiation model. We established stable ES cell lines infected with either control non-silencing shRNA (shNS) or S6K1 targetting shRNA (shS6K1). Each sample was treated with retinoic acid for 3 days to induce adipogenesis, then gene expression profile was analyzed employing microarrays and up-regulated and down-regulated genes were selected for analysis. Mouse Embryoid Bodies (approximately 1000 EBs per sample) were treated with retinoic acid (1µM) for 3 days then collected for RNA extraction and hybridization on Affimetrix microarray. Two biological replicates were each performed for EBs prepared from either shNS ESCs or shS6K1 ESCs.
2010-05-14 | E-GEOD-20349 | biostudies-arrayexpress
Project description:Analysis of CD41 single positive, VE-cadherin single positive, double positive, and double negatvie populations among 7AAD-CD45- cells from day 6 EBs Doxycline-inducible ICN1 ES cells were differentiated into EBs and ICN1 was induced from day 3-5. Non-induced or induced day 6 EBs were dissociated and subjected to FACS sorting and RNA extraction.
2010-11-14 | E-GEOD-19951 | biostudies-arrayexpress
Project description:10 biopsies from one patient undergoing a auxiliary liver and combined kidney transplantation, where one liver lobe is replaced by an auxiliary liver lobe. Thereafter the kidney is transplanted. Keywords: Time course study 10 samples, no replicates.
2011-03-02 | E-GEOD-8941 | biostudies-arrayexpress
Project description:We used a murine ES cell line in which HoxA3 expression is under control of a tetracycline-responsive element and differentiated these cells as embryoid bodies (EBs). Endothelial (Flk-1 VE-cadherin double positive, FV) and hematopoieitc progenitors (c-Kit CD41 double positive, K41) were isolated from differentiated EBs that had been induced for 6 hours by doxycycline (Dox) treatment. Here we show genes regulated upon HoxA3 upregulation (6 hours doxycycline treatment) in hematopoietic and endothelial progenitors.
2010-12-20 | E-GEOD-25080 | biostudies-arrayexpress
Project description:This experiment is part of the FunGenES project (FunGenES - Functional Genomics in Embryonic Stem Cells partially funded by the 6th Framework Programme of the European Union, http://www.fungenes.org). The experiment was conducted at University of Cologne, Cologne, Germany. Goal of the experiment was an analysis the transcriptome of the ES-cell derived pure T-brachyury expressing CGR8 cells. Materials and methods: On day 0, EBs were made from T-brachyury ES (CGR8) cell line by hanging drop protocol. On second day, the hanging drop EBs were transferred into suspension. On third day, the EBs were treated or untreated with puromycin at a concentration of 5ug/ml for 2 days. On 5th day, the medium was changed and added medium with or without puromycin at a concentration of 2 ug/ml for 1 day. On day 6th , RNA was isolated from EBs treated or untreated with puromycin for affymetrix analysis.
2010-05-12 | E-TABM-716 | biostudies-arrayexpress