Brain region and sex specific transcriptome of peripubertal stress induced adult male mice showing escalated aggression and adult female mice with no signs of aggression.
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA821699 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18556000_1.fastq.gz | Fastqsanger.gz | |||
| SRR18556000_2.fastq.gz | Fastqsanger.gz | |||
| SRR18556001_1.fastq.gz | Fastqsanger.gz | |||
| SRR18556001_2.fastq.gz | Fastqsanger.gz | |||
| SRR18556002_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 48 |
Similar Datasets
Project description:Purpose: The goal of this study is to uncover the molecular basis of peripubertal stress induced aggressive behaviour and its sex differences focussing on brain region specific transcriptome profiling (RNA-seq) and validation by quantitative reverse transcription polymerase chain reaction (qRT–PCR) Methods: Hypothalamus (Hypo) and Prefrontal cortex (PFC) mRNA profiles of 90-day-old control adult male and female and PPS exposed escalated aggressive adult male (SEagg) mice and non aggressive adult female (SNagg) were sequenced on Illumina HiSeq 2500, in 3 biological replicates.The FASTQ sequencing reads were adapter-trimmed along with a minimum length cut-off of 50 bases using Prinseq-lite. The reads were aligned to mouse genome assembly using TopHat (v.2.0.11) followed by reference-based assembly using Cufflinks (v.2.2.1). Then differentially expressing transcripts were identified using Cuffdiff (v.2.2.1). qRT–PCR validation was performed using SYBR Green assays. Results:Hypo of SEagg males showed 49 differentially expressed genes (DEGs) amongst which 28 were down-regulated, 20 were up-regulated and 1 was expressed in SEagg males but not in control males. PFC of SEagg males showed 87 DEGs amongst which 57 were downregulated, 28 were upregulated and 2 were only expressed in SEagg males but not control males. SNagg females showed 684 DEGs in Hypo and 152 DEGs in PFC when compared to their respective control samples. Conclusions: We provide the first prefrontal cortex and hypothalamus specific transcriptome profiles of peripubertal stress (PPS) exposed, Balb/c adult male mice exhibiting escalated aggression and Balb/c adult female mice showing no signs of aggression.
2022-11-02 | GSE199844 | GEO
Project description:Chronic physical aggression (CPA) is characterized by frequent use of physical aggression from early childhood to adolescence. Observed in approximately 5% of males, it is associated with early childhood adverse environments. DNA methylation, a covalent modification of DNA, regulates genome function and has been associated with early childhood adverse environments. We analyzed T cell DNA genome-wide promoter methylation profiles from two groups of adult males assessed annually for frequency of physical aggression between 6 and 15 years of age: a group with CPA and a control group. Whole genome methylation analysis was performed using MeDIP followed by hybridization to microarrays. We mapped the promoter regions of 20 000 genes and 400 microRNAs. The subjects were recruited from participants in two longitudinal studies of child development9,47. We recruited two groups of Caucasian males who were born in families with a low socioeconomic status and were living at the time of the present study within 200km from our laboratory. The first group had a history of high physical aggression from age 6 to 15 years (chronic physical aggression group, CPA). The second group was recruited from the same longitudinal studies but included only those who did not have a history of high physical aggression from age 6 to 15 (Control group). A total of 65 eligible subjects agreed to participate (8 CPA and 57 controls). Using custom-designed microarrays with 244K probes tiling the promoter regions of 20000 genes and 400 microRNAs, we obtained DNA methylation profiles by meDIP-chip. Each profile was generated in triplicate.
2013-09-30 | E-GEOD-50674 | biostudies-arrayexpress
Project description:Expression data from prepubertal, peripubertal, and adult derived mouse oocytes, and from germinal vesicle (GV), in vivo matured, and in vitro matured mouse oocytes. Oocytes derived from prepubertal females, or oocytes matured in vitro, are less developmentally competent compared to adult derived, or in vivo matured, oocytes, indicated by decreased embryonic development. One potential mechanism for decreased developmental potetential in prepubertal or in vitro matured oocytes is inadequate or inappropriate RNA degradation during oocyte maturation (progression from GV to MII). To investigate mechanisms involved in establishing oocyte cytoplasmic maturation and developmental competence, Affymetrix GeneChip microarrays were used. Keywords: Oocyte developmental competence The study encompassed three experimental designs using female B6D2F1 mice: 1) In vitro matured oocytes were obtained from d20 (prepubertal), d26 (peripubertal), and 7-8 wk old (adult) mice; 2) in vivo and in vitro matured oocytes were obtained from d26 mice; and 3) GV, in vivo matured, and in vitro matured oocytes were obtained from 7-8 wk old mice. RNA was extracted from pools of 150 oocytes and hybridized onto the Affymetrix microarrays.
2010-07-12 | E-GEOD-12432 | biostudies-arrayexpress
Project description:Chronic physical aggression (CPA) is characterized by frequent use of physical aggression from early childhood to adolescence. Observed in approximately 5% of males, it is associated with early childhood adverse environments. DNA methylation, a covalent modification of DNA, regulates genome function and has been associated with early childhood adverse environments. We analyzed T cell DNA genome-wide promoter methylation profiles from two groups of adult males assessed annually for frequency of physical aggression between 6 and 15 years of age: a group with CPA and a control group. Whole genome methylation analysis was performed using MeDIP followed by hybridization to microarrays. We mapped the promoter regions of 20 000 genes and 400 microRNAs.
2013-09-30 | GSE50674 | GEO
Project description:Expression data from prepubertal, peripubertal, and adult derived mouse oocytes, and from germinal vesicle (GV), in vivo matured, and in vitro matured mouse oocytes. Oocytes derived from prepubertal females, or oocytes matured in vitro, are less developmentally competent compared to adult derived, or in vivo matured, oocytes, indicated by decreased embryonic development. One potential mechanism for decreased developmental potetential in prepubertal or in vitro matured oocytes is inadequate or inappropriate RNA degradation during oocyte maturation (progression from GV to MII). To investigate mechanisms involved in establishing oocyte cytoplasmic maturation and developmental competence, Affymetrix GeneChip microarrays were used. Keywords: Oocyte developmental competence
2010-07-12 | GSE12432 | GEO
Project description:High frequency of physical aggression is the central feature of severe conduct disorder and is associated with a wide range of social, mental and physical health problems. We have previously tested the hypothesis that differential DNA methylation signatures in peripheral T cells are associated with a chronic aggression trajectory in males. Despite the fact that sex differences appear to play a pivotal role in determining the development, magnitude and frequency of aggression, most of previous studies focused on males, so little is known about female chronic physical aggression. We therefore tested here whether or not there is a signature of physical aggression in female DNA methylation and, if there is, how it relates to the signature observed in males. Genome-wide promoter methylation profiles of T cell DNA from adult females on a Chronic Physical Aggression (CPA, n=5) trajectory during childhood and adolescence were compared to those on normative physical aggression trajectories (NPA, n=14). Two technical replicates were generated for each individual.
2013-12-11 | E-GEOD-53192 | biostudies-arrayexpress
Project description:Animal and human studies suggest that inflammation is associated with behavioral disorders including aggression. We have recently shown that physical aggression of boys during childhood is strongly associated with reduced plasma levels of cytokines IL-1a, IL-4, IL-6, IL-8 and IL-10, later in early adulthood (Provencal et al., unpublished data). This study tests the hypothesis that there is an association between differential DNA methylation regions in cytokine genes in T cells and monocytes DNA in adult subjects and a trajectory of physical aggression from childhood to adolescence. We compared the methylation profiles of the entire genomic loci encompassing the IL-1a, IL-6, IL-4, IL10 and IL8 and three of their regulatory transcription factors (TF) NFkB1, NFAT5 and STAT6 genes in adult males on a chronic physical aggression trajectory (CPA) and males with the same background who followed a normal physical aggression trajectory (control group). We used the method of methylated DNA immunoprecipitation (MeDIP) with comprehensive cytokine gene loci and TF loci microarray hybridization, statistical analysis and false discovery rate correction. We recruited two groups of Caucasian males who were born in families with a low socioeconomic status and were living at the time of the present study within 200km from our laboratory. The first group, composed of 8 subjects, had a history of chronic physical aggression from age 6 to 15 years (chronic physical aggression group, CPA). The second group, composed of 12 subjects, was recruited from the same longitudinal studies but included only those who did not have a history of chronic physical aggression from age 6 to 15 (Control group, CG). Using custom-designed microarrays with 44K probes tiling cytokines IL-1a, IL-6, IL-4, IL10 and IL8 and three of their regulatory transcription factors (TF) NFkB1, NFAT5 and STAT6, we obtained DNA methylation profiles by meDIP-chip. Each profile was generated in triplicate.
2013-05-22 | E-GEOD-47193 | biostudies-arrayexpress
Project description:Animal and human studies suggest that inflammation is associated with behavioral disorders including aggression. We have recently shown that physical aggression of boys during childhood is strongly associated with reduced plasma levels of cytokines IL-1a, IL-4, IL-6, IL-8 and IL-10, later in early adulthood (Provencal et al., unpublished data). This study tests the hypothesis that there is an association between differential DNA methylation regions in cytokine genes in T cells and monocytes DNA in adult subjects and a trajectory of physical aggression from childhood to adolescence. We compared the methylation profiles of the entire genomic loci encompassing the IL-1a, IL-6, IL-4, IL10 and IL8 and three of their regulatory transcription factors (TF) NFkB1, NFAT5 and STAT6 genes in adult males on a chronic physical aggression trajectory (CPA) and males with the same background who followed a normal physical aggression trajectory (control group). We used the method of methylated DNA immunoprecipitation (MeDIP) with comprehensive cytokine gene loci and TF loci microarray hybridization, statistical analysis and false discovery rate correction.
2013-05-22 | GSE47193 | GEO
Project description:High frequency of physical aggression is the central feature of severe conduct disorder and is associated with a wide range of social, mental and physical health problems. We have previously tested the hypothesis that differential DNA methylation signatures in peripheral T cells are associated with a chronic aggression trajectory in males. Despite the fact that sex differences appear to play a pivotal role in determining the development, magnitude and frequency of aggression, most of previous studies focused on males, so little is known about female chronic physical aggression. We therefore tested here whether or not there is a signature of physical aggression in female DNA methylation and, if there is, how it relates to the signature observed in males. Genome-wide promoter methylation profiles of T cell DNA from adult males and females on a Chronic Physical Aggression (CPA) trajectory during childhood and adolescence were compared to adults on a normative physical aggression trajectories (NPA). Each sample was bisulphite converted gDNA pooled in equimolar amounts. Three different pools of genomic DNA were made per group: male CPA (2 or 3 different subjects per pool), male NPA (4 different subjects per pool), female CPA (2 different subjects per pool) and female NPA (4 or 5 different subjects per pool) . The Illumina Infinium 450k Human DNA methylation Beadchip was used to obtain DNA methylation profiles of the 2 groups in both sex.
2013-12-11 | E-GEOD-53191 | biostudies-arrayexpress
Project description:Modulation of action choices according to the environmental context is crucial for animal survival and reproductive success1. Aggression, despite its general importance as a social behavior2, can become detrimental if uncontrolled3,4. However, the genetic and neural basis for aggression control through active suppression remains largely unknown. Here we found nvy, a Drosophila homolog of vertebrate myeloid translocation gene (MTG)5 involved in transcriptional regulation6-8, suppresses aggression through a specific subset of neurons. Mutation of the nvy gene resulted in hyper-aggressiveness, which was rescued by neuronal expression of human MTGs as well as Drosophila nvy. The mutant exhibited persistent aggression under various contexts in which wild-type flies switch their behavioral patterns. Knockdown of nvy in octopaminergic/tyraminergic (OA/TA) neurons increased aggression, phenocopying the nvy deletion. Cell-type specific transcriptomics on OA/TA neurons derived from the nvy mutants revealed aggression-controlling genes that are likely downstream of nvy. Moreover, we found that the nvy-expressing OA/TA neuronal subpopulations specifically suppress aggression. Our results presents a powerful genetic model to unravel not only the neuronal systems that modulate aggression in a social context-dependent manner, but also the conserved molecular mechanism underlying the tumorigenesis caused by the MTG mutations.
2022-06-22 | GSE148630 | GEO