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Homo sapiens
8 Downloadable Samples
Illumina HiSeq 2500
Description
shRNA-mediated ablation of the RING-finger protein TRIM52 from multiple glioblastoma cell lines reduces proliferation and tumorigenesis. To identify gene signatures underlying this phenomenon, transcritional profile of TRIM52 knockdown cells was compared to control cells. Upon TRIM52 ablation, we find 278 differentially regulated genes. Gene ontology analysis reveals that many of the upregulated genes are associated with glycolysis and biosynthetic processes. Overall design: U87MG glioblastoma cells were stably transduced with doxycycline-inducible shRNA constructs targeting TRIM52 (two different shRNAs) or controls (two different non-targeting shRNAs). Knockdown was induced for five days using 2µg/ml doxycycline. shRNA expressing cells were sorted based on shRNA-coupled GFP expression via flow cytometry. mRNA sequening was performed in duplicate per shRNA cell line.
Publication Title
Human tripartite motif protein 52 is required for cell context-dependent proliferation.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 12 Downloadable Samples
Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
The transcription factor SRF (serum response factor) mediates epilepsy mediated gene expression
Publication Title
SRF modulates seizure occurrence, activity induced gene transcription and hippocampal circuit reorganization in the mouse pilocarpine epilepsy model.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Mus musculus
- 12 Downloadable Samples
- Illumina HiSeq 4000
Description
We sequenced whole adipose tissue from control and LCMV infected mice 6dpi, in control vs T cell-specific IFNAR knockoutmice to understand the transcriptional changes in adipose tissue upon loss of type I IFN-T cell singaling axis, and how it contributes to cachexia. Overall design: inguinal fat pad (after removing iLN) was used for sequencing in control and infected mice (LCMV clone13 2x10^6PFU), this was done in two genotypes (IFNARfl/fl) as controls, vs (IFNARfl/fl-CD4cre/+) as T-cell specific IFNAR knockouts.
Publication Title
CD8<sup>+</sup> T cells induce cachexia during chronic viral infection.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 10 Downloadable Samples
- Illumina Genome Analyzer II
Description
To fully understand cell type identity and function in the nervous system there is a need to understand neuronal gene expression at the level of isoform diversity. Here we applied Next Generation Sequencing of the transcriptome (RNA-Seq) to purified sensory neurons and cerebellar granular neurons (CGNs) grown on an axonal growth permissive substrate. The goal of the analysis was to uncover neuronal type specific isoforms as a prelude to understanding patterns of gene expression underlying their intrinsic growth abilities. Global gene expression patterns were comparable to those found for other cell types, in that a vast majority of genes were expressed at low abundance. Nearly 18% of gene loci produced more than one transcript. More than 8000 isoforms were differentially expressed, either to different degrees in different neuronal types or uniquely expressed in one or the other. Sensory neurons expressed a larger number of genes and gene isoforms than did CGNs. To begin to understand the mechanisms responsible for the differential gene/isoform expression we identified transcription factor binding sites present specifically in the upstream genomic sequences of differentially expressed isoforms, and analyzed the 3’ untranslated regions (3’ UTRs) for microRNA (miRNA) target sites. Our analysis defines isoform diversity for two neuronal types with diverse axon growth capabilities and begins to illuminate the complex transcriptional landscape in two neuronal populations. Overall design: RNA was sequenced from cultured peripheral neurons of the dorsal root ganglia (DRG neurons) and cerebellar granular neurons (CGNs) of the central nervous system
Publication Title
Isoform diversity and regulation in peripheral and central neurons revealed through RNA-Seq.
Sample Metadata Fields
Specimen part, Cell line, Subject
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SRP044619- Mus musculus
- 18 Downloadable Samples
- Illumina HiSeq 2000
Description
To identify isoform differential expression underlying peripheral nerve regeneration we performed RNA-Sequencing on DRG neurons after axotomy. Overall design: RNA was sequenced from peripheral Dorsal Root Ganglia (DRG) neurons from adult male mice 7 days after a conditioning lesion at the level of the sciatic nerve (Crushed samples) or after a sham surgery (Controls surgery).
Publication Title
Identification of miRNAs involved in DRG neurite outgrowth and their putative targets.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 6 Downloadable Samples
- Illumina HiSeq 2500
Description
Primary mammary gland stromal fibroblasts from pubertal SHARPIN-deficient cpdm/cpdm -mice and their littermate controls Overall design: mRNA seq data from 3 wt and 3 Sharpincpdm mouse mammary gland stromal fibroblast cell samples
Publication Title
SHARPIN regulates collagen architecture and ductal outgrowth in the developing mouse mammary gland.
Sample Metadata Fields
Age, Specimen part, Cell line, Subject
View Samples- Mus musculus
- 37 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Recurrent Copy Number Variations (CNVs) of human 16p11.2 have been associated with a variety of developmental/neurocognitive syndromes. In particular, deletion of 16p11.2 is found in patients with autism, developmental delay, and obesity. Patients with deletions or duplications have a wide range of clinical features, and siblings carrying the same deletion often have diverse symptoms. To study the consequence of 16p11.2 CNVs in a systematic manner, we used chromosome engineering to generate mice harboring deletion of the chromosomal region corresponding to 16p11.2, as well as mice harboring the reciprocal duplication. These 16p11.2 CNV models have dosage-dependent changes in gene expression, viability, brain architecture, and behavior. For each phenotype, the consequence of the deletion is more severe than that of the duplication. Of particular note is that half of the 16p11.2 deletion mice die postnatally; those that survive to adulthood are healthy and fertile, but have alterations in the hypothalamus and exhibit a behavior trap phenotypea specific behavior characteristic of rodents with lateral hypothalamic and nigrostriatal lesions. Our findings indicate that 16p11.2 CNVs cause both brain and behavioral anomalies, providing new insight into human neurodevelopmental disorders.
Publication Title
Dosage-dependent phenotypes in models of 16p11.2 lesions found in autism.
Sample Metadata Fields
Sex
View Samples- Mus musculus
- 48 Downloadable Samples
- Illumina HiSeq 4000
Description
SETD5, a gene linked to intellectual disability (ID) and autism spectrum disorder (ASD), is a member of the SET-domain family and encodes a putative histone methyltransferase (HMT). To date, the mechanism by which SETD5 haploinsufficiency causes ASD/ID remains an unanswered question. Setd5 is the highly conserved mouse homolog, and although the Setd5 null mouse is embryonic lethal, the heterozygote is viable. Morphological tracing and multi electrode array was used on cultured cortical neurons. MRI was conducted of adult mouse brains and immunohistochemistry of juvenile mouse brains. RNA-Seq was used to investigate gene expression in the developing cortex. Behavioral assays were conducted on adult mice. Setd5+/- cortical neurons displayed significantly reduced synaptic density and neuritic outgrowth in vitro, with corresponding decreases in network activity and synchrony by electrophysiology. A specific subpopulation of fetal Setd5+/- cortical neurons showed altered gene expression of neurodevelopment-related genes. Setd5+/- animals manifested several autism-like behaviors, including hyperactivity, cognitive deficit, and altered social interactions. Anatomical differences were observed in Setd5+/- adult brains, accompanied by a deficit of deep-layer cortical neurons in the developing brain. Our data converge on a picture of abnormal neurodevelopment driven by Setd5 haploinsufficiency, consistent with a highly penetrant risk factor. Overall design: Single cell RNA-Seq of CD24+ CD45- neuronal cells isolated from E18.5 WT or SetD5 +/- mouse fetuses.
Publication Title
Setd5 haploinsufficiency alters neuronal network connectivity and leads to autistic-like behaviors in mice.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Mus musculus
- 24 Downloadable Samples
- Illumina HiSeq 4000
Description
Truncating CHD8 mutations are amongst the highest confidence risk factors for autism spectrum disorders (ASD) identified to date. Here, we report that Chd8 heterozygous mice display increased brain size, motor delay, hypertelorism, pronounced hypoactivity, and anomalous responses to social stimuli. Whereas gene expression in the neocortex is only mildly affected at mid gestation, over 600 genes are differentially expressed in the early postnatal neocortex. Genes involved in cell adhesion and axon guidance are particularly prominent amongst the downregulated transcripts. Resting-state functional MRI identified increased synchronized activity in corticohippocampal and auditory-parietal networks in Chd8 heterozygous mutant mice, implicating altered connectivity as a potential mechanism underlying the behavioral phenotypes. Together, these data suggest that altered brain growth and diminished expression of important neurodevelopmental genes that regulate long-range brain wiring are followed by distinctive anomalies in functional brain connectivity in Chd8 +/- mice. Human imaging studies have reported altered functional connectivity in ASD patients, with long-range under-connectivity seemingly more frequent. Our data suggest that CHD8 haploinsufficiency represents a specific subtype of ASD where neuropsychiatric symptoms are underpinned by long-range over-connectivity. Overall design: RNA was isolated from microdissected cortices at E12.5 (both hemispheres) and P5 (one hemisphere and DNase-treated using the Direct-zol RNA MiniPrep kit (Zymo Research) according to the manufacturer?s instructions (n = 3 per experimental group). cDNA was end-repaired, adaptor-ligated, and A-tailed. Samples were sequenced over 2 lanes of the Illumina HiSEq 4000 platform.
Publication Title
Altered Neocortical Gene Expression, Brain Overgrowth and Functional Over-Connectivity in Chd8 Haploinsufficient Mice.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 12 Downloadable Samples
- Illumina HiSeq 2000
Description
CHD8, encoding a chromatin remodeling protein, is one of the most frequently mutated genes in autism spectrum disorders (ASDs) 1-8. However, whether and how such mutations cause autistic behaviors remain unclear. Here we show that a human CHD8 mutation causes autistic-like behaviors and enhanced excitatory drive specifically in male mice. We found that knockin mice carrying a heterozygous frame-shift mutation in the Chd8 gene (Asn2373LysfsX2) identified in human individuals with ASDs (Chd8+/N2373K mice) display male-specific autistic-like behaviors. Gene transcript analysis shows that male and female Chd8+/N2373K neurons exhibit largely opposite changes in the levels of 29 mRNAs, nine of which correspond to known ASD-risk genes. These results suggest that a human CHD8 mutation causes male-specific autistic-like behaviors in mice in association with gender-specific differential changes in gene transcripts and excitatory drive in the brain. Overall design: Whole brain transcriptome of 3 neonatal WT and CHD8 Asn2373LysfsX2 heterozygote mutant mice in both sex.
Publication Title
Sexually dimorphic behavior, neuronal activity, and gene expression in Chd8-mutant mice.
Sample Metadata Fields
Sex, Specimen part, Subject
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