Ontology highlight
ABSTRACT:
PROVIDER: PRJEB32443 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR3309780.fastq.gz | Fastqsanger.gz | |||
| ERR3309790.fastq.gz | Fastqsanger.gz | |||
| ERR3309800.fastq.gz | Fastqsanger.gz | |||
| ERR3309810.fastq.gz | Fastqsanger.gz | |||
| ERR3309820.fastq.gz | Fastqsanger.gz |
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Project description:ATP-dependent chromatin remodeling proteins are being implicated increasingly in the regulation of complex behaviors, including models of several psychiatric disorders. Here, we demonstrate that Baz1b, an accessory subunit of the ISWI family of chromatin remodeling complexes, is upregulated in the nucleus accumbens (NAc), a key brain reward region, in both chronic cocaine-treated mice and mice that are resilient to chronic social defeat stress. In contrast, no regulation is seen in mice that are susceptible to this chronic stress. Viral-mediated overexpression of Baz1b, along with its associated subunit Smarca5, in mouse NAc is sufficient to potentiate both rewarding responses to cocaine, including cocaine self-administration, and resilience to chronic social defeat stress. However, despite these similar, proreward behavioral effects, genome-wide mapping of BAZ1B in NAc revealed mostly distinct subsets of genes regulated by these chromatin remodeling proteins after chronic exposure to either cocaine or social stress. Together, these findings suggest important roles for BAZ1B and its associated chromatin remodeling complexes in NAc in the regulation of reward behaviors to distinct emotional stimuli and highlight the stimulus-specific nature of the actions of these regulatory proteins. BAZ1B (WSTF) ChIP-seq of mouse. Cocaine vs Saline, 3 biological replicates. In social defeat model: Normal control vs Susceptible vs Resilient, 3 biological replicates.
2016-07-30 | E-GEOD-85005 | biostudies-arrayexpress
Project description:Despite depression being one of the most prevalent and debilitating disorders worldwide, it has been difficult to understand its pathophysiology and to develop more effective treatments. Maladaptive transcriptional regulation within limbic neural circuits, including reward processing regions such as the nucleus accumbens (NAc), in response to chronic stress is thought to be a major contributor to the development of the syndrome. Epigenetic events?in particular, histone writers and erasers?that alter chromatin structure to regulate programs of gene expression have increasingly been associated with depression-related behavioral abnormalities in animal models and in depressed humans examined postmortem. However, very little is known about the ATP-dependent chromatin remodelers that control nucleosome positioning and the packing state of chromatin. Here we show that the ACF complex, part of the ISWI family of chromatin remodelers, is persistently and selectively upregulated in the NAc of mice that are susceptible to chronic social stress, as well as in the NAc of depressed human. We further establish that ACF induction is both necessary and sufficient for susceptibility to stress-induced depressive-like behaviors. Using ChIP-seq, we demonstrate that altered ACF binding after chronic stress is strongly correlated with altered nucleosome positioning, in particular, around the transcriptional start sites of affected genes. These alterations in ACF binding and nucleosome repositioning are associated with repressed expression of a subset of genes in animals that are susceptible to chronic stress. Together, these findings establish that active ATP-dependent chromatin remodeling by the ACF complex is a key regulator in the repression of genes that mediate susceptibility to social stress, and provide novel candidate targets for improved therapeutics of depression and other stress-related disorders. c57bl/6 mice underwent chronic social defeat stress (CSDS), and social interaction test was used to separate animals into control, susceptible and resilient groups. Nucleus accumbens (NAc) tissue was collected 48 hours after the last defeat session, and then Acf1, SNF2H ChIP-seq or H3 MNase-seq were performed based on the control, susceptible, and resilient groups. Three sequencing replicates were performed on each group.
2015-09-21 | E-GEOD-54263 | biostudies-arrayexpress
Project description:In order to better understand the effects of social stress on the prefrontal cortex, we investigated gene expression in mice subjected to acute and repeated social encounters of different duration using microarrays. The observed up-regulation of genes associated with vascular system and brain injury suggests that stressful social encounters may affect brain function through the stress-induced dysfunction of the vascular system. We studied gene expression profiles of prefrontal cortices of male mice subjected to social stress of different durations: Comparisons included: acute stress (24 hours after single social stress episode) vs. acute control (unstressed), stress-8 days vs. control-8 days, stress-13 days vs. control-13 days, stress-13 days+5 days of rest vs. control-13 days+5 days of rest. For each comparison, we analyzed 3 biological replicates per group. Two of out of three biological replicates were further replicated in dye swap (final dye swap failed due to problem during microarray hybridization). Each biological replicate consisted of equal amounts of total RNA from 3 mice subjected to the same experimental condition.
2015-01-07 | E-GEOD-64734 | biostudies-arrayexpress
Project description:Stress is a major influence on mental health status; the ways that individuals respond to or copes with stressors determine whether they are negatively affected in the future. Stress responses are established by an interplay between genetics, environment, and life experiences. Psychosocial stress is particularly impactful during adolescence, a critical period for the development of mood disorders. In this study we compared two established, selectively-bred Sprague Dawley rat lines, the “internalizing” bred Low Responder (bLR) line versus the “externalizing” bred High Responder (bHR) line, to investigate how genetic temperament and adolescent environment impact future responses to social interactions and psychosocial stress, and how these determinants of stress response interact. Animals were exposed to social and environmental enrichment in adolescence prior to experiencing social defeat and were then assessed for social interaction and anxiety-like behavior. Adolescent enrichment caused bLR rats to display less social avoidance, more social interaction, less submission during defeat, and resilience to the prolonged effects of social stress on corticosterone, while enrichment caused bHR animals to show greater aggression during defeat and during a neutral social encounter, and decreased anxiety-like behavior. To gain insight into the development of social resilience in the anxious phenotype bLRs, RNA-seq was conducted on the hippocampus and nucleus accumbens, two brain regions that mediate stress regulation and social behavior. Gene sets previously associated with stress, social behavior, aggression and exploratory activity were enriched with differential expression in both regions, with a particularly large effect on gene sets that regulate social behaviors. These findings provide further evidence that adolescent enrichment can serve as an inoculating experience against future stressors. The ability to induce social resilience in a usually anxious line of animals by manipulating their environment has translational implications, as it underscores the feasibility of intervention strategies targeted at genetically vulnerable adolescent populations.
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Project description:Social overcrowding impacts gut microbiota, promoting stress, inflammation and dysglycemia
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Project description:This study aimed to investigate the effects of depression on transcriptome in ileum using a subchronic and mild social defeat stress (sCSDS) model. In addition to exhibiting social deficit and hyperphagia-like behavior, the sCSDS mice keep much more water in their body than control mice. In order to investigate the effect of social defeat stress on not only central nervous system but also function of gastrointestinal tract, the gene expression in ileum of stressed mice was compared with control mice. We used microarrays to detail the gene expression after 10 days of social defeat stress and identified distinct classes of down-regulated genes during this process. The duration of physical contacts was set at 5 min after the first attack bite at Day 1, and then was reduced 0.5 min per day from Day 2 to Day 10.
2016-08-03 | E-GEOD-64004 | biostudies-arrayexpress
Project description:Social stress mouse models were used to simulate human post-traumatic stress disorder (PTSD). C57B/6 mice exposed to SJL aggressor mice exhibited behaviors accepted as PTSD-in-mouse phenotype: 'frozen' motion, aggressor's barrier avoidance, startled jumping, and retarded locomotion. Transcripts in spleen, blood and hemi-brain of stressed and control C57B/6 mice were analyzed using Agilent's mouse genome-wide arrays. C57B6 mice were exposed to SJL aggressor mice for periods of 5 days and 10 days (6 hours each day) to induce anxiety/stress which parallels to PTSD in human. Organs, blood and brain regions were collected after 24 hours and 1.5 week of post 5 days social defeat period; and 24 hour and 6 weeks post 10 days social stress period.
2015-12-31 | E-GEOD-68076 | biostudies-arrayexpress
Project description:We performed high-throughput profiling of gene expression in aPVT-projectors in the mPFC of DBA2/J mice subjected to subchronic and mild social defeat stress. DBA mice were subjected to 5-day of social defeat stress and then tested their social interaction and anhedonic state. After behavioral tests, mice were divided into five subtypes: SA, social interaction deficit, ANH: anhedonia, SA:ANH, both social dificit and anhedonia, RES, resilience and non-stressed (NS) control. Mice were euthanized for tissue collection. We then conducted the Immunoprecipitation and RNA-seq. Our study provided insights into the understanding of the molecular mechanisms underlying behavioral heterogeneity.
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Project description:Pig - Social Stress - Gastrointestinal Biomarkers
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