Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA107621 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The extent to which differences in germ line DNA copy number contribute to natural phenotypic variation is unknown. We analyzed the copy number content of the mouse genome to a sub-10 kb resolution. We identified over 1,300 copy number variant regions (CNVRs), most of which are < 10 kb in length, are found in more than one strain, and, in total, span 3.2% (85 Mb) of the genome. To assess the potential functional impact of copy number variation, we mapped expression profiles of purified hematopoietic stem and progenitor cells, adipose tissue and hypothalamus to CNVRs in cis. Of the more than 600 significant associations between CNVRs and expression profiles, most map to CNVRs outside of the transcribed regions of genes. In hematopoietic stem/progenitor cells, up to 28% of strain-dependent expression variation is associated with copy number variation, supporting the role of germ line CNVs as major contributors to natural phenotypic variation in the laboratory mouse.
2009-03-09 | GSE10656 | GEO
Project description:The extent to which differences in germ line DNA copy number contribute to natural phenotypic variation is unknown. We analyzed the copy number content of the mouse genome to a sub-10 kb resolution. We identified over 1,300 copy number variant regions (CNVRs), most of which are < 10 kb in length, are found in more than one strain, and, in total, span 3.2% (85 Mb) of the genome. To assess the potential functional impact of copy number variation, we mapped expression profiles of purified hematopoietic stem and progenitor cells, adipose tissue and hypothalamus to CNVRs in cis. Of the more than 600 significant associations between CNVRs and expression profiles, most map to CNVRs outside of the transcribed regions of genes. In hematopoietic stem/progenitor cells, up to 28% of strain-dependent expression variation is associated with copy number variation, supporting the role of germ line CNVs as major contributors to natural phenotypic variation in the laboratory mouse. To map the CNV content of the mouse genome, we selected 17 Tier 1-3 Mouse Phenome Project strains and three additional strains of biomedical interest, representing all major inbred lineages. We performed comparative genomic hybridization using a long-oligonucleotide array containing 2,149,887 probes evenly spaced across the reference genome with a median inter-probe spacing of 1,015 bases. Labeling, hybridization, washing and array imaging were performed as previously described (PMID:16075461). We performed segmentation using wuHMM, a Hidden Markov Model algorithm that utilizes sequence-level information and can detect CNVs less than 5 kb in length (fewer than five probes) at a low false positive rate (PMID:18334530). To estimate the overall impact of CNV on gene expression in vivo, we performed expression profiling of hematopoietic stem/progenitors cells using the Illumina Mouse Beadchip-6v1 platform. See manuscript for further details.
2009-03-08 | E-GEOD-10656 | biostudies-arrayexpress
Project description:Mouse Segmental Duplication and Copy-Number Variation
| PRJNA106591 | ENA
Project description:Recurrent DNA copy number variation in the laboratory mouse
| PRJNA102263 | ENA
Project description:Recurrent DNA copy number variation in the laboratory mouse
| PRJNA102439 | ENA
Project description:Copy number variation and gene expression in the mouse
| PRJNA107521 | ENA
Project description:Copy Number Variation in Brca2 (G25R) variant mouse tumors
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Project description:Copy number variation data in malignant mouse mammary cell lines
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Project description:The formation of hematopoietic cells relies on the chromatin remodeling activities of ISWI ATPase SMARCA5 (SNF2H) and its complexes. The Smarca5 null and conditional alleles have been used to study its functions in embryonic and organ development in mice. These mouse model phenotypes vary from embryonic lethality of constitutive knockout to less severe phenotypes observed in tissue-specific Smarca5 deletions, e.g., in the hematopoietic system. Here we show that, in a gene dosage-dependent manner, the hypomorphic allele of SMARCA5 (S5tg) can rescue not only the developmental arrest in hematopoiesis in the hCD2iCre model but also the lethal phenotypes associated with constitutive Smarca5 deletion or Vav1iCre-driven conditional knockout in hematopoietic progenitor cells. Interestingly, the latter model also provided evidence for the role of SMARCA5 expression level in hematopoietic stem cells, as the Vav1iCre S5tg animals accumulate stem and progenitor cells. Furthermore, their hematopoietic stem cells exhibited impaired lymphoid lineage entry and differentiation. This observation contrasts with the myeloid lineage which is developing without significant disturbances. Our findings indicate that animals with low expression of SMARCA5 exhibit normal embryonic development with altered lymphoid entry within the hematopoietic stem cell compartment.
2025-10-27 | PXD048865 | panorama
Project description:This is a mathematical model describing the hematopoietic lineages with leukemia lineages, as controlled by end-product negative feedback inhibition. Variables include hematopoietic stem cells, progenitor cells, terminally differentiated HSCs, leukemia stem cells, and terminally differentiated leukemia stem cells.
2024-09-02 | BIOMD0000000898 | BioModels