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SRX8707018: GSM4665750: invivo_crispr_ctrl_trim28fl_797; Mus musculus; OTHER
1 ILLUMINA (NextSeq 500) run: 34.8M spots, 9.8G bases, 4.1Gb downloads

Submitted by: NCBI (GEO)
Study: Activation of endogenous retroviruses during brain development causes neuroinflammation
show Abstracthide Abstract
Endogenous retroviruses (ERVs) make up a large fraction of mammalian genome and are thought to contribute to human disease, including brain disorders. Aberrant activation of ERVs constitute a potential trigger for neuroinflammation, but mechanistic insight into this phenomenon remains unclear. Using CRISPR/Cas9-based gene disruption of the epigenetic co-repressor protein Trim28, we found a dynamic H3K9me3-dependent regulation of ERVs in proliferating neural progenitor cells (NPCs), but not in adult neurons. In vivo disruption of Trim28 in cortical NPCs during brain development resulted in viable offspring expressing high levels of ERVs in excitatory neurons in the adult brain of mice. Neuronal ERV expression was linked to inflammation, including activated microglia, and aggregates of ERV-derived proteins. This study demonstrates that brain development is a critical period for the silencing of ERVs and provides causal in vivo evidence demonstrating that transcriptional activation of ERV in neurons results in neuroinflammation. Overall design: In vitro CRISPR Trim28-KO in mouse neural progentiro cells (NPCs) with 3 guide RNAs (guide 3, 4 and 13 targeting exon 3, 4 and 13 of Trim28) where each guide has two duplicates. Two controls (where guide RNA towards LacZ were used). In vivo CRISPR Trim28-KO (cas knockin mice): five Cas9-GFP knock in mice (referred as Cas in this document) where injected with guide RNAs 3 or 4 or 13 (targeting exon 3, 4 and 13), or all three guide RNA combined, plus one control (guideRNA towards LacZ). All guideRNAs were co-injected with AAV vectors expressing Cre. In vivo CRISPR Trim28-KO (Stop-Cas knockin mice): five stop-Cas9-GFP knock in mice (referred as StopCas in this document) where injected with AAV vectors expressing guide RNAs 3 or 4 or 13 (targeting exon 3, 4 and 13), or all three guide RNA combined, plus one control (guideRNA towards LacZ). All guideRNAs were co-injected with AAV vectors expressing Cre. In vivo Trim28-KO (Trim28-fl mice): AAV.Cre injections into Trim28-fl animals (+/- and +/+): 4 KO samples and 4 controls. In vivo Trim28-KO during development: Emx1-Cre/Trim28-fl animals. Three KOs (homozygote for Trim28-fl) and three control (heterozygote for Trim28-fl). H3K9me3 cut and run: One sample in NPCs and its respective IgGs. Trim28-KO Single cell sequencing: Two KO and two controls from the Emx mice were sequenced in single cell.
Sample: invivo_crispr_ctrl_trim28fl_797
SAMN15502830 • SRS6983705 • All experiments • All runs
Organism: Mus musculus
Library:
Instrument: NextSeq 500
Strategy: OTHER
Source: GENOMIC
Selection: other
Layout: PAIRED
Construction protocol: In vitro CRISPR: Cells were detached and resuspended in basic culture media (media excluding growth factors) with propidium iodide (1:1,000; BD Biosciences) and strained (70 mm filters, BD Biosciences). RFP+ cells were FACS isolated at 4°C (reanalysis showed >99% purity) and pelleted at 1,500 rpm for 5 min, snap frozen on dry ice and stored at -80°C until RNA/DNA were isolated. For all in vivo CRISPR experiments animals were sacrificed after two months and analyzed either by IHC or nuclei isolation (see details below) followed by DNA- or RNA-seq. Emx animals (RNAseq): Animals were sacrificed at 3 months of age for either immunohistochemistry IHC or RNA sequencing. Emx animals (single cell): The nuclei isolation was performed according to Sodersten et al. (2018). The tissue was thawed and dissociated in ice-cold lysis buffer ((0.32 M sucrose, 5 mM CaCl2, 3 mM MgAc, 0.1 mM Na2EDTA, 10 mM Tris-HCl, pH 8.0, 1 mM DTT) using a 1 ml tissue douncer (Wheaton). The homogenate was carefully layered on top of a sucrose cushion (1.8  M sucrose, 3  mM MgAc, 10  mM Tris-HCl, pH 8.0, and 1 1 mM DTT) before centrifugation at 30,000 × g for 2 hours and 15 min. Pelleted nuclei were softened for 10 minutes in 100 ml of nuclear storage buffer (15% sucrose, 10  mM Tris-_HCl, pH 7.2, 70  mM KCl, and 2  mM MgCl2) before resuspended in 300 ml of dilution buffer (10  mM Tris-_HCl, pH 7.2, 70  mM KCl, and 2  mM MgCl2) and run through a cell strainer (70 mm). Cells were run through the FACS (FACS Aria, BD Biosciences) at 4°C with low flowrate using a 100 mm nozzle (reanalysis showed >99% purity). RNAseq: Total RNA was isolated from frozen cell/nuclei pellets and brain tissue using the RNeasy Mini Kit (Qiagen) and used for RNA-seq and qPCR (tissue pieces were run in the tissue lyser for 2 min, 30 Hz, prior to RNA isolation). Single cell: 8,500 nuclei per sample were sorted via FACS and loaded onto 10X Genomics Single Cell 3' Chip along with the reverse transcription mastermix following the manufacturer's protocol for the Chromium Single Cell 3′ Library (10X Genomics, PN-120233) to generate single-cell gel beads in emulsion. cDNA amplification was done as per the guidelines from 10x Genomics and sequencing libraries were generated with unique sample indices (SI) for each sample. RNAseq libraries were generated using Illumina TruSeq Stranded mRNA library prep kit (poly-A selection) and sequenced on a NextSeq500 (PE 2 × 150bp). Cut and run (IgG and H3K9me3) library preparation was performed using the Hyper prep kit (KAPA biosystems) and sequenced on NextSeq500 2 x 75 bp. For the single cell sequencing, libraries for samples were multiplexed and sequenced on a Novaseq using a 150-cycle kit.
Experiment attributes:
GEO Accession: GSM4665750
Links:
Runs: 1 run, 34.8M spots, 9.8G bases, 4.1Gb
Run# of Spots# of BasesSizePublished
SRR1219365634,796,0119.8G4.1Gb2021-02-24

ID:
11329241

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