Kat2a regulates hippocampal memory formation [RNA-seq]
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Andre Fischer
PROVIDER: E-GEOD-53380 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Publications
K-Lysine acetyltransferase 2a regulates a hippocampal gene expression network linked to memory formation.
Stilling Roman M RM Rönicke Raik R Benito Eva E Urbanke Hendrik H Capece Vincenzo V Burkhardt Susanne S Bahari-Javan Sanaz S Barth Jonas J Sananbenesi Farahnaz F Schütz Anna L AL Dyczkowski Jerzy J Martinez-Hernandez Ana A Kerimoglu Cemil C Dent Sharon Y R SY Bonn Stefan S Reymann Klaus G KG Fischer Andre A
The EMBO journal 20140714 17
Neuronal histone acetylation has been linked to memory consolidation, and targeting histone acetylation has emerged as a promising therapeutic strategy for neuropsychiatric diseases. However, the role of histone-modifying enzymes in the adult brain is still far from being understood. Here we use RNA sequencing to screen the levels of all known histone acetyltransferases (HATs) in the hippocampal CA1 region and find that K-acetyltransferase 2a (Kat2a)--a HAT that has not been studied for its role ...[more]
Similar Datasets
Project description:We sequenced small RNAs from 12 samples extracted from mouse CA1 tissue to generate the first CA1-specific murine miRNome under normal and Kat2a-loss-of-function conditions. Samples were divded in 4 groups: A: Control (n=6), C: Kat2a cKO naïve (n=6)
2014-07-16 | E-GEOD-53427 | biostudies-arrayexpress
Project description:To gain initial insight into the regulatory mechanisms by which signalling in response to an elevated CO2 concentration exerts CA1- and CA4-dependent repression of stomatal development, we conducted high-throughput RNA-seq transcriptomics on immature aerial tissues of A. thaliana seedlings grown at the low (150 p.p.m) and elevated CO2 concentrations (500 p.p.m). Hypocotyls and cotyledons of developing seedlings (5 DAG; WT and ca1 ca4 mutant plants; n>1,000 per sample) grown in the low and elevated CO2 concentrations were used as source tissue to extract total RNA and conduct RNA-seq experiments using the HiSeq 2000 platform (Illumina). The raw data from three independent biological replicates (experiments).
2014-09-24 | E-MTAB-4447 | biostudies-arrayexpress
Project description:Olfactory ensheathing cells are one of the few central nervous system regenerative cells discovered so far. It is characterized by its lifelong nerve regeneration function, and it can also release a variety of neurotrophic factors and neural adhesion molecules. It is considered to be the glial cell with the strongest myelination ability. Olfactory ensheathing cells and Schwann cells have phenotypes in common, they can promote axon regeneration(R. Doucette, 1995). Olfactory ensheathing cells have the characteristics of Schwann cells and astrocytes, but the overall performance tends to be the former, which has two unique characteristics. First, it exists not only in the peripheral nerves (Schwann cells), but also in the central nervous system (astroglia); second, the olfactory mucosa has the ability to regenerate life-long, including human olfactory ensheathing cells(J. C. Bartolomei and C. A. Greer, 2000). Regeneration is a process in which olfactory ensheathing cells participate in efficient regulation, although the specific mechanism is not yet clear. Olfactory ensheathing cells are different from astrocytes and Schwann cells, but at the same time have the characteristics of these two cells(S. C. Barnett, 2004), like Schwann cells help axon growth, but more than Schwann cells It can make axons grow long distances, that is, it has stronger migration(A. Ramon-Cueto et al., 1998); there are also astrocytes that have a nutritional effect on the survival of neurons and the growth of axons, but olfactory ensheathing cells can also wrap neurons forms myelin sheath to support the growth of nerve processes(R. Devon and R. Doucette, 1992; J. Gu et al., 2019). There are two characteristics that make olfactory ensheathing cells the best choice for the treatment of neurological diseases(S. C. Chiu et al., 2009; J. Kim et al., 2018; M. Abdel-Rahman et al., 2018). Olfactory ensheathing cells are gradually used to treat spinal cord injuries and have shown amazing effects(J. C. Bartolomei and C. A. Greer, 2000; K. J. Liu et al., 2010; R. Yao et al., 2018). Olfactory ensheathing cells that have been used in research are usually derived from the olfactory bulb(E. H. Franssen et al., 2007), but it is easier to obtain olfactory ensheathing cells from the olfactory mucosa in clinical practice(M. Ryszard et al., 2006), so the difference between the olfactory ensheathing cells from the olfactory bulb and the olfactory mucosa There are more and more studies(B. M. U. et al., 2007), and previous studies have shown that they not only have many similar functions, but also have many differences(M. W. Richter et al., 2005; L. Wang et al., 2014; K. E. Smith et al., 2020). Because olfactory ensheathing cells derived from the olfactory bulb are not easy to obtain, olfactory ensheathing cells derived from the olfactory mucosa have become the focus of attention. Although we know that olfactory ensheathing cells from two sources have nerve repair functions, it is not clear why the two different sources of olfactory ensheathing cells have different therapeutic effects. Nicolas G. once studied that the genetic difference between the two cells and found that there are many genes related to wound repair and nerve regeneration(G. Nicolas et al., 2010). We have reason to guess that olfactory ensheathing cells from these two sources will also have a large difference in protein level. Our research group wants to use the current mature transcriptome and proteomic sequencing technologies to explore the difference between olfactory ensheathing cells from the olfactory bulb and olfactory mucosa, and explain why the two sources of olfactory ensheathing cells shows different therapeutic effects, hope to provide a new theoretical basis for future clinical treatment.
2022-02-16 | PXD024046 | Pride
Project description:The wide application of pig disease model has caused a surge of interest in the study ofderivation of pig induced pluripotent cells (iPSCs). Here we performed genome-wide analysis of gene expression profiling by RNA-seq and small RNA-seq and DNA methylation profile by MeDIP-seq in pig iPSCs through comparison with somatic cells. We identified mRNA and microRNA transcripts that were specifically expressed in pig iPSCs. Our analysis identifies the genes up-regulated in pig iPS compared with somatic cells and also the differentially expressed genes between pig iPSCs under different culture medium. We then pursued comprehensive bioinformatics analyses, including functional annotation of the generated data within the context of biological pathways, to uncover novel biological functions associated with maintenance of pluripotency in pig. This result supports that pig iPS have transcript profiles linked to M-bM-^@M-^\ribosomeM-bM-^@M-^], M-bM-^@M-^\chromatin remodelingM-bM-^@M-^], and genes involved in M-bM-^@M-^\cell cycle M-bM-^@M-^\that may be critical to maintain their pluripotency, plasticity, and stem cell function. Our analysis demonstrates the key role of RNA splicing in regulating the pluripotency phenotype of pig cells. Specifically, the data indicate distinctive expression patterns for SALL4 spliced variants in different pig cell types and highlight the necessity of defining the type of SALL4 when addressing the expression of this gene in pig cells. MeDIP-seq data revealed that the distribution patterns of methylation signals in pig iPS and somatic cells along the genome. We identify 25 novel porcine miRNA, including pluripotency-related miR-302/367cluster up-regulated in pig iPSCs. At last, we profile the dynamic gene expression signature of pluripotent genes in the preimplantation development embryo of pig. The resulting comprehensive data allowed us to compare various different subsets of pig pluripotent cell. This information provided by our analysis will ultimately advance the efforts at generating stable naM-CM-/ve pluripotency in pig cells.
2015-09-17 | E-MTAB-2634 | biostudies-arrayexpress
Project description:We sequenced mRNA from 24 samples extracted from mouse CA1 tissue to generate the first CA1-specific murine transcriptome and the first CA1-transcriptome in response to environmental novelty under normal and Kat2a-loss-of-function conditions.
2014-07-16 | GSE53380 | GEO
Project description:Psoriasis and atopic dermatitis (AD) are characterized by polarized CD4+ T cell responses. During the polarization of naM-CM-/ve CD4+ T cells, DNA methylation plays an important role in the regulation of gene transcription. In this study, we profiled the genome-wide DNA methylation status of naM-CM-/ve CD4+ T cells in patients with psoriasis or AD and healthy controls using a ChIP-seq method. As a result, twenty-six regions in the genome ranging in size from 10 to 70 kb were markedly hypomethylated in patients with psoriasis. These regions were mostly pericentromeric on 10 different chromosomes and overlapped with various strong epigenomic signals, such as histone modifications and transcription factor binding sites, that were observed in the ENCODE project. Gene-centric analysis indicated that the promoter regions of 124 genes on the X chromosome had dramatically elevated methylation levels in patients with psoriasis as compared to those from healthy controls (> 4-fold). Moreover, immune-related genes on the X chromosome had higher hypermethylation than other genes (P < 0.05). These findings imply that methylation changes in naM-CM-/ve CD4+ T cells may affect CD4+ T cell polarization, especially in the pathogenesis of psoriasis. Keywords: Psoriasis, Atopic dermatitis, DNA methylation, naM-CM-/ve CD4+ T cells Sample submission examines DNA methylation from human naive CD4+ T cells in patients with psoriasis and atopic dermatitis. Note: Raw data available only for Sample GSM871288.
2012-03-17 | E-GEOD-35582 | biostudies-arrayexpress
Project description:We propose to definitively characterise the somatic genetics of ER+ve, HER2-ve breast cancer through generation of comprehensive catalogues of somatic mutations in breast cancer cases by high coverage genome sequencing coupled with integrated transcriptomic and methylation analyses.
2013-01-30 | E-ERAD-145 | biostudies-arrayexpress
Project description:In this study we identify Mettl3, an m6A RNA modification writer, as a critical regulator for terminating naM-CM-/ve pluripotency and a positive maintainer of primed pluripotency in vitro and in vivo. Remarkably, Mettl3 knockout pre-implantation epiblasts and naM-CM-/ve ES cells, entirely lack m6A on coding mRNAs and are viable. Yet, they fail to adequately terminate the naM-CM-/ve pluripotent state, and subsequently undergo aberrant priming and early lineage commitment at the post-implantation stage. A comprehensive functional and genomic analysis involving profiling of m6A, RNA transcription and translation in Mettl3 wild-type and knockout pluripotent and differentiated cells, identified m6A as a critical determinant that destabilizes secondary naM-CM-/ve specific pluripotency genes Esrrb, Klf4 and Nanog, and restrains their transcript stability and translation efficiency. In summary, our findings provide for the first time evidence for a critical role for an mRNA epigenetic modification in early mammalian development in vivo, and identify a mechanism that functionally regulates mouse naM-CM-/ve and primed pluripotency in an opposing manner. m6A-seq was measured from total RNA in mouse embryonic stem cells (ESCs), embroid bodies (EBs) and embronic fibroblasts (MEF). 3 biological replicates are available from BVSC ESC line and EBs, and two biological replicates are available for MEFs. Each sample consist of IP to m6A and control input
2014-11-02 | E-GEOD-61995 | biostudies-arrayexpress
Project description:NaM-CM-/ve, liver- and gut-activated CD8 OT-I T cells show differential migration behaviour. To analyze which genes could be responsible for different migration patterns, naM-CM-/ve, liver-activated and gut-activated CD8 T cells were isolated and compared for their gene expression profile. Gene expression profiles of naM-CM-/ve CD8 OT-I T cells versus liver-activated T cells and gut-activated T cells, respectively. NaM-CM-/ve CD8 OT-I T cells were isolated from lymph nodes and spleens of OT-I mice. CD8 OT-I T cells activated by liver-derived and gut-derived antigen for three days in vivo, positive for CFSE were sorted from livers of TF-OVA mice or from mesenteric lymph nodes of iFABP-OVA mice. After total RNA extraction, reverse transcription, cDNA extraction, the biotinylated cRNA was transcribed, fragmented, and 15 M-BM-5g cRNA hybridized in duplicates for each of the three groups to the GeneChip arrays. Group1: naM-CM-/ve, Group2: liver-activated Group3: gut-activated. Lists of differentially regulated genes were created using High Performance Chip Data Analysis (HPCDA) with Bioretis database (http://www.bioretis-analysis.de). Worldwide data sharing is possible via Bioretis, please ask the authors.
2014-02-25 | E-GEOD-39449 | biostudies-arrayexpress
Project description:Here we modeled T-ALL resistance to Notch inhibition, identifying M-bM-^@M-^XpersisterM-bM-^@M-^Y cells that readily expand in the presence of gamma secretase inhibitor (GSI) and the absence of Notch signaling. Rare persister cells are already present in naM-CM-/ve T-ALL populations, and the reversibility of the phenotype is suggestive of an epigenetic mechanism. Relative to GSI-sensitive cells, persisters activate distinct signaling and gene expression programs, and exhibit global chromatin compaction. A shRNA screen identified chromatin regulators whose depletion preferentially impairs persister cell viability, including BRD4, an acetyl-histone reader. BRD4 is up-regulated in the persisters and binds enhancers near genes with critical functions in T-ALL, including MYC and BCL2. Treatment of persisters with the BRD4 inhibitor JQ1 down-regulates these targets and induces growth arrest and apoptosis, at doses well tolerated by GSI-sensitive cells. Prompted by these findings, we examined and established the efficacy of GSI M-bM-^@M-^S JQ1 combination therapy against primary human leukemias in vivo. Our findings establish a role for epigenetic heterogeneity in leukemia drug resistance and suggest the potential of combination therapies that include epigenetic modulators to prevent and treat resistant disease. Examination of 5 different histone modifications and BRD4 in the T cell leukemia cell lines DND-41 and KOPT-K1 after chronic treatment with gamma Secretase inhibitor (Compound E, 1 uM, EMD4 Bioscience; persister) or vehicle (naM-CM-/ve).
2014-03-01 | E-GEOD-54379 | biostudies-arrayexpress