Mouse Inbred Strain Variation Muscle
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE662 | GEO | 2003/12/10
SECONDARY ACCESSION(S): PRJNA87597
REPOSITORIES: GEO
Similar Datasets
Project description:Variation in gene expression profiles was determined between mouse inbred strains in hindlimb muscle tissue. Strains under investigation were: C57Bl/6, C57Bl/10, CBA, DBA2, and BALB/c.
2003-12-09 | E-GEOD-662 | biostudies-arrayexpress
Project description:Analysis of the pulmonary gene expression in two mouse strains BALB/cOlaHsd (BALB/c) and CBA/CaOlaHsd (CBA/Ca) after infection with various serotypes of Streptococcus pneumoniae. BALB/c mice show high resistance to infection with S. pneumoniae strain D39 (serotype 2), while CBA/Ca mice are highly susceptible. The lung samples of BALB/c and CBA/Ca were collected at 6h post-infection with one of the tested pneumococcal serotypes (2, 3, 6B and 19F) and for control animals (PBS-treated). Additionally lung samples from both mouse strains were collected at 12h and 24h post-infection with pneumococcal strain D39. The lists of differentially expressed genes were created by the comparison of infected versus PBS-treated animals and infected BALB/c versus infected CBA/Ca for each pneumococcal strain. The tested hypotheses were: 1) infection with S. pneumoniae will change the pulmonary transcriptomes of both mouse strains 2) The pulmonary gene expression will be specific for mouse strains and for the pneumococcal serotype and 3) The change in the pulmonary gene expression will associate with future clinical outcome of infection or with the type of observed inflammatory responses.
2015-10-28 | GSE61459 | GEO
Project description:Copy number variants were determined in 3-5 males from 13 inbred laboratory mouse strains and 21 Mus musculus individuals caught in various geographic locations, using Nimblegen 385k arrays. CopyMap was used to predict CNVs. 3-5 males from 13 inbred strains and 21 Mus musculus caught in various geographic locations were compared to a single C57BL/6J individual by array comparative genome hybridisation.
2010-12-31 | E-GEOD-24424 | biostudies-arrayexpress
Project description:Gene expression profiling in C57BL/6J and A/J mouse inbred strains reveals gene networks specific for brain regions independent of genetic background Comparison of whole genome expression data of amygdala and hippocampus of both C57BL/6J and A/J mouse inbred strains using a network approach
2010-01-28 | GSE17955 | GEO
Project description:Because activation of the immune response is dependent on extensive changes in gene expression, it is likely that a major component of inter-individual variation in the immune response is ultimately mediated at the level of gene regulation. Here, we examine the influence of genetic variation on inducible gene expression in the murine immune response. We extracted primary CD4 splenocytes from inbred strains A/J, C57BL/6J, BALB/c, DBA/2J, and 129x1/SvJ (3 animals/strain) and measured mRNA transcript levels using microarrays in both basal state and four hours after stimulation with PMA/Ionomycin. We report strain-specific genome-wide differences in mRNA expression between A/J, Balb/c, C57BL/6J, DBA/2J and 129X1/SvJ inbred mice in CD4 splenocytes in basal, stimulated (4hr, PMA/I) states.
2019-09-23 | GSE36551 | GEO
Project description:Analysis of the pulmonary gene expression in two mouse strains BALB/cOlaHsd (BALB/c) and CBA/CaOlaHsd (CBA/Ca) after infection with various serotypes of Streptococcus pneumoniae. BALB/c mice show high resistance to infection with S. pneumoniae strain D39 (serotype 2), while CBA/Ca mice are highly susceptible. The lung samples of BALB/c and CBA/Ca were collected at 6h post-infection with one of the tested pneumococcal serotypes (2, 3, 6B and 19F) and for control animals (PBS-treated). Additionally lung samples from both mouse strains were collected at 12h and 24h post-infection with pneumococcal strain D39. The lists of differentially expressed genes were created by the comparison of infected versus PBS-treated animals and infected BALB/c versus infected CBA/Ca for each pneumococcal strain. The tested hypotheses were: 1) infection with S. pneumoniae will change the pulmonary transcriptomes of both mouse strains 2) The pulmonary gene expression will be specific for mouse strains and for the pneumococcal serotype and 3) The change in the pulmonary gene expression will associate with future clinical outcome of infection or with the type of observed inflammatory responses. Total RNA obtained from lung tissue from BALB/cOlaHsd and CBA/CaOlaHsd mouse strains (Harlan) post intranasal infection with Streptococcus pneumoniae of various serotypes (2, 3, 6B and 19F) dose 5.0E06 CFU or PBS-treated animals
2015-10-28 | E-GEOD-61459 | biostudies-arrayexpress
Project description:Humans vary markedly in their propensity to develop asthma, despite often being exposed to similar environmental stimuli. Similarly, mouse strains vary in susceptibility to airways pathology in experimental asthma. Sensitization and aerosol challenge with ovalbumin (OVA) induces eosinophil accumulation, mucus production and airways obstruction in BALB/c and C57BL/6 mice. In contrast, CBA/Ca mice show relatively little pathology. Allergen-induced production of IL-4, IL-5, IL-10 and IFN-g was detected in all three strains, with BALB/c mice generating the highest levels of IL-4, IL-5 and IL-10. Microarray analysis was used to identify genes differentially regulated in lung tissue after OVA challenge. Differentially regulated genes in the lungs of the asthma-susceptible C57BL/6 and BALB/c strains numbered 242 and 145, respectively, whereas only 42 genes were differentially expressed in the resistant CBA/Ca strain. In C57BL/6 mice, transcripts were enriched for adhesion molecules and this was associated with high levels of eosinophil recruitment. Differentially regulated genes in the lungs of only the asthma-susceptible strains numbered 64 and several of these have not previously been associated with asthma. Many of the genes differentially regulated in the susceptible strains were enzymes involved in inflammation. Using network analysis, mRNA for the anti-apoptotic protein survivin was found to be up-regulated in the lungs following allergen challenge. Survivin mRNA and protein were also expressed at high levels in eosinophils recovered by bronchoalveolar lavage from BALB/c and C57BL/6 mice. We propose that rapid apoptosis of lung eosinophils due to low expression of survivin contributes to the limitation of pathology in CBA/Ca mice Humans vary markedly in their propensity to develop asthma, despite often being exposed to similar environmental stimuli. Similarly, mouse strains vary in susceptibility to airways pathology in experimental asthma. Sensitization and aerosol challenge with ovalbumin (OVA) induces eosinophil accumulation, mucus production and airways obstruction in BALB/c and C57BL/6 mice. In contrast, CBA/Ca mice show relatively little pathology. Allergen-induced production of IL-4, IL-5, IL-10 and IFN-g was detected in all three strains, with BALB/c mice generating the highest levels of IL-4, IL-5 and IL-10. Microarray analysis was used to identify genes differentially regulated in lung tissue after OVA challenge. Differentially regulated genes in the lungs of the asthma-susceptible C57BL/6 and BALB/c strains numbered 242 and 145, respectively, whereas only 42 genes were differentially expressed in the resistant CBA/Ca strain. In C57BL/6 mice, transcripts were enriched for adhesion molecules and this was associated with high levels of eosinophil recruitment. Differentially regulated genes in the lungs of only the asthma-susceptible strains numbered 64 and several of these have not previously been associated with asthma. Many of the genes differentially regulated in the susceptible strains were enzymes involved in inflammation. Using network analysis, mRNA for the anti-apoptotic protein survivin was found to be up-regulated in the lungs following allergen challenge. Survivin mRNA and protein were also expressed at high levels in eosinophils recovered by bronchoalveolar lavage from BALB/c and C57BL/6 mice. We propose that rapid apoptosis of lung eosinophils due to low expression of survivin contributes to the limitation of pathology in CBA/Ca mice
2009-06-15 | GSE15414 | GEO
Project description:Humans vary markedly in their propensity to develop asthma, despite often being exposed to similar environmental stimuli. Similarly, mouse strains vary in susceptibility to airways pathology in experimental asthma. Sensitization and aerosol challenge with ovalbumin (OVA) induces eosinophil accumulation, mucus production and airways obstruction in BALB/c and C57BL/6 mice. In contrast, CBA/Ca mice show relatively little pathology. Allergen-induced production of IL-4, IL-5, IL-10 and IFN-g was detected in all three strains, with BALB/c mice generating the highest levels of IL-4, IL-5 and IL-10. Microarray analysis was used to identify genes differentially regulated in lung tissue after OVA challenge. Differentially regulated genes in the lungs of the asthma-susceptible C57BL/6 and BALB/c strains numbered 242 and 145, respectively, whereas only 42 genes were differentially expressed in the resistant CBA/Ca strain. In C57BL/6 mice, transcripts were enriched for adhesion molecules and this was associated with high levels of eosinophil recruitment. Differentially regulated genes in the lungs of only the asthma-susceptible strains numbered 64 and several of these have not previously been associated with asthma. Many of the genes differentially regulated in the susceptible strains were enzymes involved in inflammation. Using network analysis, mRNA for the anti-apoptotic protein survivin was found to be up-regulated in the lungs following allergen challenge. Survivin mRNA and protein were also expressed at high levels in eosinophils recovered by bronchoalveolar lavage from BALB/c and C57BL/6 mice. We propose that rapid apoptosis of lung eosinophils due to low expression of survivin contributes to the limitation of pathology in CBA/Ca mice Humans vary markedly in their propensity to develop asthma, despite often being exposed to similar environmental stimuli. Similarly, mouse strains vary in susceptibility to airways pathology in experimental asthma. Sensitization and aerosol challenge with ovalbumin (OVA) induces eosinophil accumulation, mucus production and airways obstruction in BALB/c and C57BL/6 mice. In contrast, CBA/Ca mice show relatively little pathology. Allergen-induced production of IL-4, IL-5, IL-10 and IFN-g was detected in all three strains, with BALB/c mice generating the highest levels of IL-4, IL-5 and IL-10. Microarray analysis was used to identify genes differentially regulated in lung tissue after OVA challenge. Differentially regulated genes in the lungs of the asthma-susceptible C57BL/6 and BALB/c strains numbered 242 and 145, respectively, whereas only 42 genes were differentially expressed in the resistant CBA/Ca strain. In C57BL/6 mice, transcripts were enriched for adhesion molecules and this was associated with high levels of eosinophil recruitment. Differentially regulated genes in the lungs of only the asthma-susceptible strains numbered 64 and several of these have not previously been associated with asthma. Many of the genes differentially regulated in the susceptible strains were enzymes involved in inflammation. Using network analysis, mRNA for the anti-apoptotic protein survivin was found to be up-regulated in the lungs following allergen challenge. Survivin mRNA and protein were also expressed at high levels in eosinophils recovered by bronchoalveolar lavage from BALB/c and C57BL/6 mice. We propose that rapid apoptosis of lung eosinophils due to low expression of survivin contributes to the limitation of pathology in CBA/Ca mice
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Project description:It is well established that epigenetic features, such as histone modifications and DNA methylation, are associated with gene expression across cell types. However, it is not well known how variation in genotype affects epigenetic state, or to what extent such variation contributes to variation in gene expression across genetically distinct individuals. Here we investigated the relationship between heritable epigenetic variation and gene expression in hepatocytes across nine inbred mouse strains. Eight of the inbred strains were founders of the diversity outbred (DO) mice, and the ninth was DBA/2J, which, along with C57BL/6J, is one of the founders of the BxD recombinant inbred panel of mice. We surveyed four histone modifications, H3K4me1, H3K4me3, H3K27me3 and H3K27ac, as well as DNA methylation. We used ChromHMM to identify 14 chromatin states representing distinct combinations of the four measured histone modifications. We found that variation in chromatin state mirrored genetic variation across the inbred strains. Furthermore, epigenetic variation was correlated with gene expression across strains. The correspondence between epigenetic state and gene expression was replicated in an independent population of DO mice in which we imputed local epigenetic state. In contrast, we found that DNA methylation did not vary across inbred strains and was not correlated with variation in expression in DO mice. This work suggests that chromatin state is highly influenced by local genotype and may be a primary mode through which expression quantitative trait loci (eQTLs) are mediated. We further demonstrate that strain variation in chromatin state, paired with gene expression is useful for annotation of functional regions of the mouse genome. Finally, we provide a data resource that documents variation in chromatin state across genetically distinct individuals.
2022-09-25 | GSE213967 | GEO
Project description:It is well established that epigenetic features, such as histone modifications and DNA methylation, are associated with gene expression across cell types. However, it is not well known how variation in genotype affects epigenetic state, or to what extent such variation contributes to variation in gene expression across genetically distinct individuals. Here we investigated the relationship between heritable epigenetic variation and gene expression in hepatocytes across nine inbred mouse strains. Eight of the inbred strains were founders of the diversity outbred (DO) mice, and the ninth was DBA/2J, which, along with C57BL/6J, is one of the founders of the BxD recombinant inbred panel of mice. We surveyed four histone modifications, H3K4me1, H3K4me3, H3K27me3 and H3K27ac, as well as DNA methylation. We used ChromHMM to identify 14 chromatin states representing distinct combinations of the four measured histone modifications. We found that variation in chromatin state mirrored genetic variation across the inbred strains. Furthermore, epigenetic variation was correlated with gene expression across strains. The correspondence between epigenetic state and gene expression was replicated in an independent population of DO mice in which we imputed local epigenetic state. In contrast, we found that DNA methylation did not vary across inbred strains and was not correlated with variation in expression in DO mice. This work suggests that chromatin state is highly influenced by local genotype and may be a primary mode through which expression quantitative trait loci (eQTLs) are mediated. We further demonstrate that strain variation in chromatin state, paired with gene expression is useful for annotation of functional regions of the mouse genome. Finally, we provide a data resource that documents variation in chromatin state across genetically distinct individuals.
2022-09-25 | GSE213966 | GEO