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Transcriptomics of Ts65Dn mice with viral-mediated overexpression of miR-200b

ABSTRACT: This project aims to identify transcriptomic changes in the Down Syndrome mouse model (Ts65Dn) in two brain regions, hippocampus and preoptic area. Also, we aim to identify possible transcriptomics rescue effect in Ts55Dn with viral-mediated overexpression of miR200. In total, we have 3 groups of hippocampal and 3 groups of preotic area tissue (WT control virus, 65Dn control virus and 65Dn miR200 - N=4 per group).

ORGANISM(S): Mus musculus

PROVIDER: GSE199974 | GEO | 2023/05/23

REPOSITORIES: GEO

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Transcriptomics of Ts65Dn mice with viral-mediated overexpression of miR-200b

Project description:Transcriptomics of Ts65Dn mice with viral-mediated overexpression of miR-200b

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Gene expression profile at single nuclei level of hippocampal neurons from WT and Ts65Dn mice

Project description:In order to characterize the cellular and molecular alterations associated with DS hippocampal dysfunction, given the rich neural cell diversity of this brain region, we used single nucleus RNA sequencing to dissect transcriptional dysregulation associated with specific cell types in the DS mouse model Ts65Dn

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Cell-specific gene expression profiling of warm-sensitive neurons

Project description:TRAP-seq gene expression profiling. GFP-L10a is expressed in BDNF+ or PACAP+ in preoptic area. Bdnf+ or Pacap+ cells in the preoptic area are labelled with GFP-L10a fusion protein expression to study cell-type specific gene expression. We used adult BDNF-Cre (custom generated, discussed in submitted paper) and Pacap-Cre mice (Allen Brain Institute, gift Hongkui Zeng) and injected Cre-depndent adenoassociated virus (AAV2-EF1a-DIO-EGFP-L10a, custom made) into the ventromedial preoptic area.

2016-09-12 | GSE80120 | GEO

Lentiviral vector-based microRNA sponges identifies miR-155 and miR-802 target genes in the hippocampus of Ts65Dn mice

Project description:A major challenge in Down syndrome (DS) is to understand how the extra-dose of functional chromosome 21 (HSA21) genetic elements can impact on the tissue-specific transcriptome to contribute to phenotypic alterations. MiRNAs are post-transcriptional modulators with genome-wide regulatory effects. Five microRNAs have been identified in HSA21 that are present in triple copy in DS individuals. Interestingly, in the Ts65Dn mouse model of DS two of these miRNAs, miR-155 and miR-802, are also triplicated resulting in its overexpression. In the current work, we have developed a lentiviral miRNA-sponge genetic strategy for miR-155 and miR-802 (Lv-miR155-802T) to identify novel mRNA targets involved in hippocampal function. Hippocampal injection of the lentiviral sponge in Ts65Dn mice reduced miR-155 and miR-802 overexpression. Noticeable lentiviral sponge rescued the expression of the miRNA predicted targets showing the potential of the strategy to identify miRNA dosage-sensitive genes with potential involvement in DS-hippocampal phenotypes.

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The impact of Mmu17 non-Hsa21 orthologous genes in the Ts65Dn mouse model of Down syndrome: the “gold standard” refuted

Project description:Background: Despite successful preclinical treatment studies to improve neurocognition in the Ts65Dn mouse model of Down syndrome (DS), translation to humans has failed. This raises questions about the appropriateness of the Ts65Dn mouse as the “gold standard” for DS research. Here we used the novel Ts66Yah mouse that carries both an extra chromosome and the identical segmental Mmu16 trisomy as Ts65Dn without the Mmu17 non-orthologous region. Methods: Forebrains from embryonic day 18.5 Ts66Yah and Ts65Dn mice, along with euploid littermate controls, were used for gene expression and pathway analyses. Behavioral experiments were performed in neonatal and adult mice. Since male Ts66Yah mice are fertile, parent of origin transmission of the extra chromosome was studied. Results: We mapped 45 protein coding genes to the Ts65Dn Mmu17 non-orthologous, among which 71-82 % are expressed during forebrain development. Several of these genes were uniquely overexpressed in Ts65Dn embryonic forebrain; this produced major differences in dysregulated genes and pathways. Despite these genome-wide differences, the primary Mmu16 trisomic effects were highly conserved in both models, resulting in several commonly dysregulated disomic genes and pathways. Delays in motor development, communication and olfactory spatial memory were present in Ts66Yah but more pronounced in Ts65Dn neonates. Adult Ts66Yah mice showed working memory deficits and sex-specific effects in exploratory behavior and spatial hippocampal memory, while long-term memory was preserved. These deficits were milder when compared to Ts65Dn mice. Conclusions: Our findings suggest that triplication of the non-orthologous Mmu17 genes significantly contributes to the phenotype of the Ts65Dn mouse and may explain why preclinical trials that used this model have unsuccessfully translated to human therapies.

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Transcription profiling of Ts65Dn vs control mice in nine different mouse tissues

Project description:To understand the molecular basis of Down syndrome pathogenesis, we performed a transcriptome analysis of nine different tissues in Ts65Dn, an established mouse model of human trisomy 21. Ts65Dn mice have segmental trisomy of mouse chromosome 16 with ca. 128 genes at dosage imbalance (Reeves et al. 1995). The Ts65Dn mouse is widely used as a model for studies of DS because it is at dosage imbalance for the orthologs of about half the 284 Chr21 genes. Ts65Dn mice have several features that directly parallel developmental anomalies of DS. We compare here the expression of 136 mouse orthologs of Chr21 genes, 77 of which are triplicated in Ts65Dn, in trisomic and euploid mice. We designed a mouse cDNA expression array interrogating 136 mmu21 genes. RNA pools from four adult male Ts65Dn mice and four male euploid littermates were prepared from cortex and dissected from three to four month-old mice. Directly labeled first strand cDNA probes from nine different tissues were hybridized to the arrays in replicated hybridizations. A total of 446 genes that are not triplicated in Ts65Dn mice served as controls. These included 62 mmu21 genes from MMU10, MMU17, and non-triplicated portions of MMU16, plus 384 randomly distributed mouse cDNAs from the Unigene collection.

2004-04-23 | E-MEXP-102 | biostudies-arrayexpress

Transcriptome from mouse Ts65Dn adult hippocampi and entorhinal cortices

Project description:We have created the Ts66Yah a new model for Down syndrome or T21, derived from the Ts65Dn. Ts66Yah does not contain a set of genes present in 3 copies that are not linked to T21. On this model (Ts66), we performed an RNA seq analysis on 2 structures (hippocampus and entorhinal cortex, ref: S18276) and we have done the same experiment on the Ts65Dn line to compare the 2 models. For this we sampled the hippocampus (hippo) and the entorhinal cortex (EntCortex) from 6 wild-type control male littermate animals and 6 males trisomic individual (Ts66 or Ts65).

2022-09-20 | GSE213500 | GEO

Mandibular precursor at E13.5 in Ts65Dn Down syndrome mouse

Project description:Gene expression of mandibular precursor from embryonic day 13.5 trisomic and euploid embryos from the Ts65Dn Down syndrome mouse model. Results provide insight into importance of non-trisomic genes in organogenesis.

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Affymetrix expression arrays from heart extracted RNA in Ts65Dn and Ms5Yah and Ts65DnMs5Yah mouse models

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2011-10-05 | E-MEXP-3355 | biostudies-arrayexpress

Mandibular precursor at E13.5 in Ts65Dn Down syndrome mouse

2010-11-02 | E-GEOD-24554 | biostudies-arrayexpress