ArticleGenome research2008
Genomic copy number and expression variation within the C57BL/6J inbred mouse strain.
Article in Genome research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.
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Who cites it
69 citing papers in PubMed.
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- SNPs, short tandem repeats, and structural variants are responsible for differential gene expression across C57BL/6 and C57BL/10 substrains.Cell genomics · 2022Article
- Metabolic differences and differentially expressed genes between C57BL/6J and C57BL/6N mice substrains.PloS one · 2022Article
- Defective folate metabolism causes germline epigenetic instability and distinguishes Hira as a phenotype inheritance biomarker.Nature communications · 2021Article
- Extensive genome-wide duplications in the eastern oyster (Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2021Article
- PHACTR1 genetic variability is not critical in small vessel ischemic disease patients and PcomA recruitment in C57BL/6J mice.Scientific reports · 2021Article
- Major oscillations in spontaneous home-cage activity in C57BL/6 mice housed under constant conditions.Scientific reports · 2021Article
- Challenges and opportunities for strain verification by whole-genome sequencing.Scientific reports · 2020Article
- The abiding relevance of mouse models of rare mutations to psychiatric neuroscience and therapeutics.Schizophrenia research · 2020Article
- Epithelial Membrane Protein 2 (EMP2) Promotes VEGF-Induced Pathological Neovascularization in Murine Oxygen-Induced Retinopathy.Investigative ophthalmology & visual science · 2020Article
- Six-Gene Signature Associated with Immune Cells in the Progression of Atherosclerosis Discovered by Comprehensive Bioinformatics Analyses.Cardiovascular therapeutics · 2020Article
- Influence of allelic differences in Down syndrome.Progress in brain research · 2020Review
- Altered Levels of Proteins and Phosphoproteins, in the Absence of Early Causative Transcriptional Changes, Shape the Molecular Pathogenesis in the Brain of Young Presymptomatic Ki91 SCA3/MJD Mouse.Molecular neurobiology · 2019Article
- The Genome of C57BL/6J "Eve", the Mother of the Laboratory Mouse Genome Reference Strain.G3 (Bethesda, Md.) · 2019Article
9 more citing papers are in PubMed but not listed here.
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Authors and funding
2 authors.
Funding
Abstract
The C57BL/6J strain is one of the most widely used animal models for biomedical research, and individual mice within the strain are often assumed to be genetically identical after more than 70 yr of inbreeding. Using a single nucleotide polymorphism (SNP) genotyping panel, we assessed if copy number variations (CNVs) could be detected within the C57BL/6J strain by comparing relative allele frequencies in first generation (F(1)) progeny of C57BL/6J mice. Sequencing, quantitative PCR, breeding, and array comparative genomic hybridization (CGH) together confirmed the presence of two CNVs. Both CNVs span genes encoded on chromosome 19, and quantitative RT-PCR demonstrated that they result in altered expression of the insulin-degrading enzyme (Ide) and fibroblast growth factor binding protein 3 (Fgfbp3) genes. Analysis of 39 different C57BL/6J breeders revealed that 64% of mice from the Jackson Laboratory colony were heterozygous for the CNV spanning Ide. Homozygotes with and without the duplication were present in concordance with Hardy-Weinberg equilibrium (13% and 23%, respectively), and analysis of archived samples from the C57BL/6J colony suggests that the duplication has rapidly reached a high frequency in the colony since 1994. The identification of two CNVs in the small portion of the genome screened demonstrates that individual mice of highly inbred strains are not isogenic and suggests other CNVs may be segregating within C57BL/6J as well as other carefully maintained inbred strains. These differences can influence interpretations of physiological, biomedical, and behavioral experiments and can be exploited to model CNVs apparent in the human genome.
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