Genome-wide DNA methylation analysis in peripheral blood of monozygotic twins informative for psychopathology
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE120307 | GEO | 2018/09/22
REPOSITORIES: GEO
Similar Datasets
Project description:Human intelligence demonstrates one of the highest heritabilities among human quantitative traits. Phenotypically discordant monozygotic twins provide a way to identify loci responsible for normal-range intelligence. We conducted array-based genome-wide gene expression analysis aiming to identify genes displaying significant difference among monozygotic twin pairs manifesting between-co-twins IQ differences. Total RNA was isolated from B-lymphoblastoid cell lines and applied to Affymetirx arrays after reverse transcription. 17 twin pairs (34 subjects) were recruited in this study.
2012-10-20 | E-GEOD-33476 | biostudies-arrayexpress
Project description:DNA methylation appears to play an essential mechanistic role in the pathogenesis of ALL, thereby potentiate its use as a biomarker for diagnosis and prognosis (Milani, Lundmark et al. 2010; Geng, Brennan et al. 2012; Sandoval, Heyn et al. 2013), and even a potential target of novel therapeutic approaches in ALL. In present study, we collected blood specimens for 4 pairs of monozygotic twins (MZ) and 1 pair of dizygotic twin (DZ) that are discordant for ALL. We sought to comprehensively assess the magnitude of genetic and epigenetic differences between ALL-affected and unaffected twins. we conducted whole genome and whole methylome sequencing on these five pairs of ALL-discordant twins. We also examined both the MZ and DZ twins using whole-genome bisulfite sequencing (WGBS). At first, the methylation differences across the genome were addressed globally by Circos software. And then tried to characterize the co-twin methylation divergence in specific genomic regions between ALL-discordant twin pairs. These patterns of dynamic co-twin methylation changes in these discordant ALL samples were generally consistent among MZ and DZ twins, indicating similarities of methylation abnormalities. As a result, 780, 566, 309, 293 and 2110 DMRs were identified, with a similar distribution pattern across different genomic elements among the five twin pairs.Then we annotate whether these DMRs were located in regulatory elements and identification of genes with recurring methylation alterations in a cohort of ALL patients. We collected blood specimens from 4 pairs of MZ twins and 1 pair of DZ twin that are discordant for ALL. At first, the methylation differences across the genome were addressed globally by Circos software. And then tried to characterize the co-twin methylation divergence in specific genomic regions and differentially methylated gene regions (DMRs) were identified between ALL-discordant twin pairs. Then we annotate whether these DMRs were located in regulatory elements and identification of genes with recurring methylation alterations in a cohort of ALL patients.
2015-01-01 | E-GEOD-59869 | biostudies-arrayexpress
Project description:DNA methylation data for 479 women from 130 families including 66 monozygotic twin pairs, 66 dizygotic twin pairs and 215 sisters of twins.
2017-06-21 | GSE100227 | GEO
Project description:Natural variation in gene expression among healthy human individuals has been largely unexplored. In order to understand the genetic basis of variation in gene expression between normal human individuals, we need to obtain genome-wide expression data from various populations. Studies in monozygotic twins could enable us to estimate the size of the contribution of genetic and environmental factors to the natural variation in gene expression. In this work, we report the gene expression analysis of 5 pairs of monozygotic twins and 3 unrelated individuals Normal healthy twin pairs were recruited for the study. Three more normal individuals including two females and one male were recruited. First, labeled products were hybridized with the Affymetrix GeneChip Test3 arrays. If the results were judged satisfactory, hybridization was subsequently carried out with the HG U95A arrays as per manufacturer's instructions. Arrays were hybridized at 45°C for 16 hours. The array was then washed using an automated Gene Chip Fluidics Station 400. After washing, the array was stained with streptavidin-phycoerythrin and scanned with a HP Gene Array Scanner. The data was analyzed using Gene Chip Software for expression analysis (MAS 5). All Gene Chip experiments were performed at the Weizmann Institute of Science, Rehovot, Israel. Following comparisons were carried out: 1. Between female identical twin pair (GSM14480 and GSM14481; GSM29053 and GSM 29054; GSM 29055 and GSM 29056) 2. Between male identical twin pair (GSM14478 and GSM14479; GSM 29057 and GSM 29058) 3. Between unrelated female individuals (include GSM14483, GSM20645 also but exclude comparisons within same twin pairs) 4. Between unrelated male individuals (include GSM14477 but exclude comparisons between same twin pairs) Keywords: repeat sample
2004-12-31 | GSE928 | GEO
Project description:By integrating data on the immune profiles of healthy monozygotic and dizygotic twin pairs we estimated the variance in CD25 expression by naïve Th cells to be largely driven by genetic and shared early environmental influences. Nonetheless, the Th cell subset expanded in MS twins, which was also elevated in non-twin MS patients , emerged independent of the individual genetic makeup. These cells expressed CNS-homing receptors, exhibited a dysregulated CD25-IL-2 axis, and their proliferative capacity positively correlated with MS severity . Together, the pair-matched analysis of the extended twin approach allowed us to discern genetically- and environmentally- determined features of an MS-associated immune signature.
2022-01-13 | GSE193181 | GEO
Project description:Objective: To identify genes involved in idiopathic absence epilepsies by analysing gene expression using a monozygotic (MZ) twin design. Methods: Genome-wide gene expression in lymphoblastoid cell lines was determined using microarrays derived from five discordant and four concordant MZ twin pairs with idiopathic absence epilepsies and five unaffected MZ twin pairs. Gene expression was analysed using three strategies: discordant MZ twins were compared as matched pairs, MZ twins concordant for epilepsy were compared to control MZ twins, and a singleton design of affected versus unaffected MZ twin individuals was used irrespective of twin pairing. An overlapping gene list was generated from these analyses. Dysregulation of genes recognised from the microarray experiment were validated using quantitative real time PCR (qRT-PCR) in the twin sample and in an independent sample of 18 sporadic absence cases and 24 healthy controls. Results: Sixty-five probe sets were identified from the microarray analysis strategies. Sixteen genes were chosen for validation and nine of these genes confirmed by qRT-PCR in the twin sample. Differential expression of the immediate early gene EGR1 and RCN2, coding for the calcium-binding protein Reticulocalbin 2, was re-confirmed by qRT-PCR in the independent sample. Interpretation: Using a unique sample of discordant MZ twins, our study identified genes with altered expression, which suggest novel mechanisms in idiopathic absence epilepsy. Dysregulation of EGR1 and RCN2 might represent common transcriptional alterations in idiopathic absence epilepsy. Keywords: Childhood Absence Epilepsy, Juvenile Absence Epilepsy, Idiopathic Generalised Epilepsy, gene expression, twin study, monozygotic twins
2008-02-28 | GSE7486 | GEO
Project description:Schizophrenia affects approximately 1% of the world population. Genetics, epigenetics, and environmental factors are known to play a role in this psychiatric disorder. While there is a high concordance in monozygotic twins, about half of twin pairs are discordant for schizophrenia. To address the question of how and when concordance in monozygotic twins occur, we have obtained fibroblasts from two pairs of schizophrenia discordant twins (one sibling with schizophrenia while the second one is unaffected by schizophrenia) and three pairs of healthy twins (both of the siblings are healthy). We have prepared iPSC models for these 3 groups of patients with schizophrenia, unaffected co-twins, and the healthy twins. When the study started the co-twins were considered healthy and unaffected but both the co-twins were later diagnosed with a depressive disorder. The reprogrammed iPSCs were differentiated into hippocampal neurons to measure the neurophysiological abnormalities in the patients. We found that the neurons derived from the schizophrenia patients were less arborized, were hypoexcitable with immature spike features, and exhibited a significant reduction in synaptic activity with dysregulation in synapse-related genes. Interestingly, the neurons derived from the co-twin siblings who did not have schizophrenia formed another distinct group that was different from the neurons in the group of the affected twin siblings but also different from the neurons in the group of the control twins. Importantly, their synaptic activity was not affected. Our measurements that were obtained from schizophrenia patients and their monozygotic twin and compared also to control healthy twins point to hippocampal synaptic deficits as a central mechanism in schizophrenia
2024-05-06 | GSE263672 | GEO
Project description:Human intelligence demonstrates one of the highest heritabilities among human quantitative traits. Phenotypically discordant monozygotic twins provide a way to identify loci reponsible for the phenotypical differences. We performed comprehensive DNA methylation analysis in monozygotic twins manifesting differences in IQ scores. Genes with significantly different methylation status are considered as candidates related to human intelligence. Methylation profiling was conducted using methylated DNA enriched fraction by MethylMiner. Subjects were compared with their co-twins by MAT software and bed files were generated. Significantly high methyalted regions with MAT score p value < 0.000001 in each twin pairs were extracted as candidates.
2012-10-20 | E-GEOD-33477 | biostudies-arrayexpress
Project description:Objective:; To identify genes involved in idiopathic absence epilepsies by analysing gene expression using a monozygotic (MZ) twin design. Methods:; Genome-wide gene expression in lymphoblastoid cell lines was determined using microarrays derived from five discordant and four concordant MZ twin pairs with idiopathic absence epilepsies and five unaffected MZ twin pairs. Gene expression was analysed using three strategies: discordant MZ twins were compared as matched pairs, MZ twins concordant for epilepsy were compared to control MZ twins, and a singleton design of affected versus unaffected MZ twin individuals was used irrespective of twin pairing. An overlapping gene list was generated from these analyses. Dysregulation of genes recognised from the microarray experiment were validated using quantitative real time PCR (qRT-PCR) in the twin sample and in an independent sample of 18 sporadic absence cases and 24 healthy controls. Results:; Sixty-five probe sets were identified from the microarray analysis strategies. Sixteen genes were chosen for validation and nine of these genes confirmed by qRT-PCR in the twin sample. Differential expression of the immediate early gene EGR1 and RCN2, coding for the calcium-binding protein Reticulocalbin 2, was re-confirmed by qRT-PCR in the independent sample. Interpretation:; Using a unique sample of discordant MZ twins, our study identified genes with altered expression, which suggest novel mechanisms in idiopathic absence epilepsy. Dysregulation of EGR1 and RCN2 might represent common transcriptional alterations in idiopathic absence epilepsy. Experiment Overall Design: Genome-wide gene expression in lymphoblastoid cell lines was determined using microarrays derived from five discordant and four concordant MZ twin pairs with idiopathic absence epilepsies and five unaffected MZ twin pairs.
2008-04-07 | E-GEOD-7486 | biostudies-arrayexpress
Project description:In this study, we profiled the placental proteome of IUGR twins and normal cotwins from 6 monochorionic twin pairs with selective intrauterine growth restriction (sIUGR).
2022-07-15 | PXD035369 |