RNAseq after cortical spreading depolarization (SD)
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE214623 | GEO | 2022/10/05
REPOSITORIES: GEO
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Project description:Activation of neurons is one of the fundamental events for the functioning of nervous system. Neuronal activation relays information to next neurons. On the other hand, the activated neurons themselves are also influenced by neuronal activation. Depending on the type and condition of neuronal activation, these activated neurons change their gene expressions, thereby being able to process information more or less efficiently. We applied the microarray technology to identify hither-to-uncharacterized as activity-dependent genes. Especially, we screened the transcription factors, because early changes in the transcription factors should result in alterations of gene expression profiles and subsequent neuronal properties. Experiment Overall Design: Rat primary cortical neurons with or without KCl treatment were selected for RNA extraction and hybridization on Affymetrix microarrays. To identify the genes whose expression was induced by depolarization, we first compared gene expression profiles in control vs. 4 hr after KCl (25 mM) treated cortical neurons using Affymetrix Genechips specified for neurobiology. All four hybridizations were analyzed for correlation accuracy between the replicates of the same treatments .Control replicates (control 1, 2) KCl-treated replicates (KCl 1, 2)
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2024-07-16 | PXD045078 | Pride
Project description:Preterm children are frequently exposed to various painful stimuli in the early days of life. Early-life-pain (ELP) may affect cortical development and reduce the fitness and resilience in during youth and adult life. We developed an optogenetic Cre/loxP mouse model of "early-life-pain" (ELP) using mice with transgenic expression of an improved channelrhodopsin-2 (ChR2)/Td-Tomato fusion protein under control of the advillin promoter, that drives expression of ChR2/td-Tomato specifically in primary somatosensory neurons of the dorsal root ganglia (Avil-ChR2 mice). Floxed ChR2/td-Tomato littermates (ChR2-flfl) were used as controls. Mice were exposed to blue light in a chamber once daily from postnatal day P1-P5. Cortical gene expression was analyzed at P7 via RNA-sequencing in eight biological replicates per group. Cortices were rapidly excised and snap froze in liquid nitrogen. Total RNA was extracted from with Qiagen RNeays spin columns and quantified on a Nanodrop. Sequencing libraries were prepared using Illumina TruSeq stranded mRNA library preparation kit, and sequencing was performed on an Illumina NGS platform. The alignment was performed with SeqMan NGen 17 (Lasergene) using the reference genome mm10 provided from UCSC (GRCm38) as template, a minimum read length of 35 bp and automatic adapter trimming. Sequence reads were normalized with EdgeR and analyzed in ArrayStar 17 (Lasergene). Differential gene expression was assessed with general linear models and adjusted according to Benjamini Hochberg.
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2008-10-26 | E-GEOD-11256 | biostudies-arrayexpress
Project description:Background Segmental duplications (SDs) are not evenly distributed along chromosomes. The reasons for this biased susceptibility to SD insertion are poorly understood. Accumulation of SDs is associated with increased genomic instability, which can lead to structural variants and genomic disorders such as the Williams-Beuren syndrome. Despite these adverse effects, SDs have become fixed in the human genome. Focusing on chromosome 7, which is particularly rich in interstitial SDs, we have investigated the distribution of SDs in the context of evolution and the three dimensional organisation of the chromosome in order to gain insights into the mutual relationship of SDs and chromatin topology. Results Intrachromosomal SDs preferentially accumulate in those segments of chromosome 7 that are homologous to marmoset chromosome 2. Although this formerly compact segment has been re-distributed to three different sites during primate evolution, we can show by means of public data on long distance chromatin interactions that these three intervals, and consequently the paralogous SDs mapping to them, have retained their spatial proximity in the nucleus. Focusing on SD clusters implicated in the aetiology of the Williams-Beuren syndrome locus we demonstrate by cross-species comparison that these SDs have inserted at the borders of a topological domain and that they flank regions with distinct DNA conformation. Conclusions Our study suggests a link of nuclear architecture and the propagation of SDs across chromosome 7, either by promoting regional SD insertion or by contributing to the establishment of higher order chromatin organisation themselves. The latter could compensate for the high risk of structural rearrangements and thus may have contributed to their evolutionary fixation in the human genome.
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2017-05-23 | GSE79108 | GEO
Project description:This experiment comprises RNA-seq data used to study evolutionary differences between humans and mice in neuronal activity-dependent transcriptional responses. Activity-dependent transcriptional responses in developing human stem cell-derived cortical neurons were compared with those induced in developing primary- or stem cell-derived mouse cortical neurons 4 hours after KCl-induced membrane depolarisation. Activity-dependent transcriptional responses were also measured in aneuploid mouse neurons carrying human chromosome 21, allowing study of the regulation of Hsa21 genes, plus their mouse orthologs, side-by-side in the same cellular environment of a mouse primary neuron.
2017-02-16 | E-MTAB-5489 | biostudies-arrayexpress
Project description:Background: The forskolin-induced swelling assay (FIS) in intestinal organoids (IOs), used to determine in vitro responsiveness to elexacaftor/tezacaftor/ivacaftor (ETI), showed variability in swelling among IOs obtained from people with CF (pwCF) carrying the same genotype. We aimed to characterise the effect of ETI on the transcriptional activity of IOs-derived cells to understand the intracellular processes triggered by ETI and the differences in treatment response. Methods: Six high- and six low-responding IOs to ETI, derived from F508del/F508del pwCF, were incubated with or without ETI for 2 to 6 hours. Gene expression was modelled using negative binomial models adjusted for subjects, having time and incubation with ETI as predictors. Results: Incubation with ETI resulted in a significant upregulation of several biological processes: mostly related to chemokines and signalling, chemotaxis, and tissue development processes. No changes were observed in abundance of the CFTR transcripts or in CFTR-related gene sets and pathways. The genes and pathways associated with ETI did not overlap with those whose expression changed with time only. IOs with a high FIS response did not significantly differ in any interpretable gene from the FIS-low organoids. Conclusions: The changes in the IOs gene expression upon the exposure to ETI cannot explain differences in the magnitude of IOs FIS-measured response to ETI. Genes of the CFTR-related pathways do not change their transcriptional activity; instead, overexpression was observed in genes of inflammatory-like cytokine response and receptor activation pathways, seemingly unrelated to the mechanisms of FIS, but possibly related to the effect of ETI itself.
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Project description:Background Segmental duplications (SDs) are not evenly distributed along chromosomes. The reasons for this biased susceptibility to SD insertion are poorly understood. Accumulation of SDs is associated with increased genomic instability, which can lead to structural variants and genomic disorders such as the Williams-Beuren syndrome. Despite these adverse effects, SDs have become fixed in the human genome. Focusing on chromosome 7, which is particularly rich in interstitial SDs, we have investigated the distribution of SDs in the context of evolution and the three dimensional organisation of the chromosome in order to gain insights into the mutual relationship of SDs and chromatin topology. Results Intrachromosomal SDs preferentially accumulate in those segments of chromosome 7 that are homologous to marmoset chromosome 2. Although this formerly compact segment has been re-distributed to three different sites during primate evolution, we can show by means of public data on long distance chromatin interactions that these three intervals, and consequently the paralogous SDs mapping to them, have retained their spatial proximity in the nucleus. Focusing on SD clusters implicated in the aetiology of the Williams-Beuren syndrome locus we demonstrate by cross-species comparison that these SDs have inserted at the borders of a topological domain and that they flank regions with distinct DNA conformation. Conclusions Our study suggests a link of nuclear architecture and the propagation of SDs across chromosome 7, either by promoting regional SD insertion or by contributing to the establishment of higher order chromatin organisation themselves. The latter could compensate for the high risk of structural rearrangements and thus may have contributed to their evolutionary fixation in the human genome. 2 cell lines-5 samples: 2x DNA fragmentation during apoptosis; 3x ChIP (2x H4K8ac, 1x H3) IMR90: 1x DNA fragmentation during apoptosis; 1x H4K8ac ChIP. Both hybridized on a custom designed 4x 180k oligonucleotide microarray
2014-07-01 | E-GEOD-41356 | biostudies-arrayexpress