Shank3(∆C/+) mice exhibit altered transcriptomic response to swim stress
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA728364 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14473000_1.fastq.gz | Fastqsanger.gz | |||
| SRR14473000_2.fastq.gz | Fastqsanger.gz | |||
| SRR14473001_1.fastq.gz | Fastqsanger.gz | |||
| SRR14473001_2.fastq.gz | Fastqsanger.gz | |||
| SRR14473002_1.fastq.gz | Fastqsanger.gz |
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Project description:Shank3 is a postsynaptic protein that complexes with group 1 metabotropic, AMPA-, and NMDA-type glutamate receptors. Mutations of Shank3 are causal for Phelan-McDermid syndrome (PMS) and associated autism phenotypes. Individuals with PMS often exhibit sensitivity to novelty or stress that can result in behavioral deterioration. Here we use a Shank3 mouse model with face-validity to PMS [Shank(3∆C/+)] and perform a transcriptomic analysis of principal neurons from neocortex of mice subjected to brief swim stress. Analysis reveals overrepresented pathways related to synapses accompanied by elevated expression of the immediate early gene Homer1a. In normal brain Homer1a is dynamically expressed in association with motivated behavior and mediates an essential step in sleep-related homeostatic down-scaling of synaptic proteins. This is consistent with observations that synaptic Shank3 expression requires Homer cross-linking, which is interrupted by Homer1a. Accentuated Homer 1a expression in Shank3(∆C/+) results in marked reductions of Shank3 expression, changes in synapse composition and NMDA-dependent synaptic plasticity, and disruption of social motivation. Deletion of Homer1a partially mitigates stress-induced phenotypes in Shank3(∆C/+) mice. Homer 1a is required for developmental plasticity, learning and memory, yet its enhanced expression in Shank3(∆C/+) may underlie a vulnerability of PMS patients that highlights the challenge of clinical management.
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Project description:We used microarrays to identify the gene with altered expression in the hippocampus of depression mouse model with forced swim stress campared to control mice .
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Project description:Shank3 is an abundant excitatory postsynaptic scaffolding proteins implicated in various neurodevelopmental and psychiatric disorders, including ASD, Phelan-McDermid syndrome, intellectual disability, and schizophrenia. Shank3-mutant mice with a homozygous deletion of exons 14-16 (Shank3-HM mice) show ASD-like behavioral deficits and altered synaptic and neuronal functions, but little is known about how different ages, brain regions, and gene dosages contribute to transcriptomic phenotypes in these mice. Here, we performed RNA-Seq-based transcriptomic analyses of the prefrontal cortex, hippocampus, and striatum in adult Shank3 heterozygous- and homozygous-mutant mice. In addition, juvenile and adult Shank3 homozygous-mutant forebrain transcriptomes were compared. Juvenile and adult forebrain transcriptomes from Shank3 homozygous-mutant mice showed the patterns that are opposite and similar to those observed in ASD: reverse-ASD and ASD-like patterns, respectively. Here, the juvenile reverse-ASD pattern involved synaptic gene upregulations and ribosomal and mitochondrial downregulations, whereas the adult ASD-like pattern involved opposite changes. Gene set enrichment analyses (GSEA) of brain regional transcripts in adult Shank3-HT and Shank3-HM mice revealed that the cortical, hippocampal, and striatal transcripts show distinctly altered biological functions and ASD-related/risk gene expressions. The cortex and striatum display ASD-like patterns whereas the hippocampus displays reverse-ASD patterns. The cortical ASD-like pattern more strongly involves ASD-risk genes whereas the striatal ASD-like pattern more strongly involves astrocyte/microglia genes. Shank3-HT and Shank3-HM transcripts in a given brain region display largely similar patterns in biological functions and ASD-related/risk gene expressions, suggestive of small gene dosage effects. These results suggest that heterozygous and homozygous Shank3 deletions in mice lead to age, brain region, and gene dosage-differential transcriptomic changes.
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Project description:Shank3 is an abundant excitatory postsynaptic scaffolding proteins implicated in various neurodevelopmental and psychiatric disorders, including ASD, Phelan-McDermid syndrome, intellectual disability, and schizophrenia. Shank3-mutant mice with a homozygous deletion of exons 14-16 (Shank3-HM mice) show ASD-like behavioral deficits and altered synaptic and neuronal functions, but little is known about how different ages, brain regions, and gene dosages contribute to transcriptomic phenotypes in these mice. Here, we performed RNA-Seq-based transcriptomic analyses of the prefrontal cortex, hippocampus, and striatum in adult Shank3 heterozygous- and homozygous-mutant mice. In addition, juvenile and adult Shank3 homozygous-mutant forebrain transcriptomes were compared. Juvenile and adult forebrain transcriptomes from Shank3 homozygous-mutant mice showed the patterns that are opposite and similar to those observed in ASD: reverse-ASD and ASD-like patterns, respectively. Here, the juvenile reverse-ASD pattern involved synaptic gene upregulations and ribosomal and mitochondrial downregulations, whereas the adult ASD-like pattern involved opposite changes. Gene set enrichment analyses (GSEA) of brain regional transcripts in adult Shank3-HT and Shank3-HM mice revealed that the cortical, hippocampal, and striatal transcripts show distinctly altered biological functions and ASD-related/risk gene expressions. The cortex and striatum display ASD-like patterns whereas the hippocampus displays reverse-ASD patterns. The cortical ASD-like pattern more strongly involves ASD-risk genes whereas the striatal ASD-like pattern more strongly involves astrocyte/microglia genes. Shank3-HT and Shank3-HM transcripts in a given brain region display largely similar patterns in biological functions and ASD-related/risk gene expressions, suggestive of small gene dosage effects. These results suggest that heterozygous and homozygous Shank3 deletions in mice lead to age, brain region, and gene dosage-differential transcriptomic changes.
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Project description:Shank3 is a core excitatory postsynaptic protein enriched in the striatum. We have previously generated and characterized Shank3-overexpressing transgenic mice, and found that these mice exhibited manic-like behavioral phenotypes. To understand molecular mechanisms underlying the behavioral changes, we performed transcriptome (RNA-sequencing) analysis of the striatal tissues from 12-week-old wild-type and Shank3 transgenic mice.
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Project description:Shank3 is a core excitatory postsynaptic protein expressed in multiple brain regions including the medial prefrontal cortex, striatum, and hippocampus. We have previously generated and characterized Shank3-overexpressing transgenic mice, and found that these mice exhibited manic-like behavioral phenotypes and increased food intake. To understand molecular mechanisms underlying the behavioral changes, we performed transcriptome (RNA-sequencing) analysis of the hypothalamic tissues from 10 to 12-week-old wild-type and Shank3 transgenic mice.
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Project description:Genome-wide microarray analysis of the effects of swim-training on zebrafish larval development. Zebrafish were subjected to swim-training from 5 days post fertilization (dpf) until 10 dpf. Subsequently, we performed a genome-wide microarray analysis of trained and control fish at 10 dpf. The goal of the project was to investigate the effects of swim-training on the gene expression level during zebrafish larval development
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Project description:Shank3 is a core excitatory postsynaptic protein expressed in multiple brain regions including the medial prefrontal cortex, striatum, and hippocampus. Shank3 knock-out mice display autism-like behaviors and synaptic dysfunction. To understand molecular mechanisms underlying the behavioral and synaptic changes, we performed transcriptome (RNA-sequencing) analysis of the striatum tissues from 10 to 12-week-old wild-type and Shank3 knock-out/heterozygous mice.
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Project description:Shank3 is a core excitatory postsynaptic protein expressed in multiple brain regions including the medial prefrontal cortex, striatum, and hippocampus. We have previously generated and characterized Shank3-overexpressing transgenic mice, and found that these mice exhibited manic-like behavioral phenotypes. To understand molecular mechanisms underlying the behavioral changes, we performed transcriptome (RNA-sequencing) analysis of the mPFC tissues from 10 to 12-week-old wild-type and Shank3 transgenic mice.
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Project description:Genome-wide microarray analysis of the effects of swim-training on zebrafish larval development. Zebrafish were subjected to swim-training from 5 days post fertilization (dpf) until 10 dpf. Subsequently, we performed a genome-wide microarray analysis of trained and control fish at 10 dpf. The goal of the project was to investigate the effects of swim-training on the gene expression level during zebrafish larval development Two-condition experiment: control vs trained fish. RNA was isolated from 10 control fish and from 10 trained fish. Subsequently, each sample was labeled with Cy3 and Cy5 in order to correct for dye bias. Control-Cy3 and Trained-Cy5 were hybridized on array 1 and Trained-Cy5 and Control-Cy3 were hybridized on array 2.
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