Gene expression profiles of in vitro-infected (Leishmania major) and uninfected mouse bone marrow-derived macrophages
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE17550 | GEO | 2009/09/04
SECONDARY ACCESSION(S): PRJNA118549
REPOSITORIES: GEO
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Project description:Gene expression profiles of in vitro-infected (Leishmania major) and uninfected bone-marrow-derived macrophages from BALB/c, C57BL/6, C.B6-(lmr1, lmr2) and B6.c-(lmr1, lmr2) mouse strains. We utilised microarrays to investigate a number of issues. Firstly, we determined which genes were differentially regulated in macrophages in response to infection with Leishmania major. Secondly, we hoped to gain some insight into the differences between C-B6-(lmr1, lmr2) congenic mice and their parental control BALB/c, as well as differences between B6-c-(lmr1, lmr2) and their parental control C57BL/6. This would aid us in the search for the genes underlying our loci, since the only genomic regions differing between the two strains are those of the two congenic intervals on chromosomes 9 and 17. Any genes differentially regulated would be contributing to the experimental infection differences observed between the congenic mice and their parental controls. Experiment Overall Design: L. major-infected and uninfected bone marrow-derived macrophages from C57BL/6, BALB/c, B6.c-(lmr1, lmr2) and C.B6-(lmr1, lmr2) mice were analyzed. Macrophages from 6 mice were pooled for each sample.
2009-09-13 | E-GEOD-17550 | biostudies-arrayexpress
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2022-11-04 | GSE217040 | GEO
Project description:Inbred congenic strain B6.C6.132.54/Vad was created using C57BL/6ByJ background and BALB/cJ donor strains. Flanking background markers at chr. 6: 75.9 Mb (rs4226008, NCBI Mouse Build 36 / dbSNP Build 126) and 122.3 Mb (rs3023093), and limiting donor markers at 81.9 Mb (rs4226024) and at 91.8 Mb (rs3712161) defined the introgressed region. We concluded the segment size must be between 9.9 Mb and 46.4 Mb. In a Quantitative Trait Gene identification study we compared brain (without cerebellum) gene expression between progenitors and congenics. Such comparisons can facilitate identification of cis-regulated genes and to establish genetic control of a complex phenotype whose expression is associated with the introgressed chromosome segment. We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of up-regulated genes during this process. Keywords: strain comparison
2007-07-30 | GSE7155 | GEO
Project description:Natural variation in protein expression is common in all organisms and contribute to phenotypic differences among individuals. While variation in gene expression at the transcript level has been extensively investigated, the genetic mechanisms underlying variation in protein expression have lagged considerably behind. Here we investigate genetic architecture of protein expression by profiling a deep mouse brain proteome of two inbred strains, C57BL/6J (B6) and DBA/2J (D2), and their reciprocal F1 hybrids using two-dimensional liquid chromatography coupled with tandem mass spectrometry (LC/LC-MS/MS) technology. By comparing protein expression levels in the four mouse strains, we observed 329 statistically significant differentially expressed proteins between the two parental strains and identified four common inheritance patterns, including dominant, additive, over- and under-dominant expression. We further applied the proteogenomic approach to detect variant peptides and define protein allele-specific expression (pASE).
2021-11-01 | PXD025830 | Pride
Project description:We identified a congenic mouse with an introgressed region from the A/J donor inbred strain on an inbred C57BL/6J background that showed a reduced locomotor stimulant response to methamphetamine. We conducted microarray analysis of the striatum from drug-naive female and male mice that were 6-9 weeks old. The congenic region is on chromosome 11 and spans approximately 84-96 Mb. There were two groups of mice used in the analysis: B6 control mice versus congenic mice. Congenic mice were collapsed across heterozygous and homozygous genotypes. All mice are on a C57BL/6J background. Congenic mice differ only on chromosome 11 where they contain the introgressed A/J alleles from 84-96 Mb. 14 C57BL/6J wildtype mice and 14 B6.A/J congenic mice (84-96 Mb region from A/J strain) were examined for gene expression differences using striatal tissue (left and right punches pooled). All mice were drug-naïve and were 6-9 weeks old at the time of sacrifice.
2012-01-18 | E-GEOD-35139 | biostudies-arrayexpress
Project description:We have analyzed the differential expression between the obesity model lean congenic B6.C-D7Mit353 (1) and the background C57BL/6J strains, in four different tissues of male mice: Brain, GWAT (Gonadal White Adipose Tissue), liver and muscle (gastrocnemius). From the 32,381 mouse genes covered by the Applied Biosystems AB1700 microarray system, we identified 330 genes passing FDR at 5% and 188 genes passing FDR at 1%, in any one of the four tissues examined. None of the genes that passed FDR testing were in the congenic donor region. 65 genes from the 8 megabases congenic region were assayed; only six genes (Thrsp, Kctd14, Myo7a, Capn5, Dgat2 and Mtap6) passed statistical significance filtering but not FDR filtering. (1) Diament & Warden 2004: PMID 14569280. Keywords: Congenic mice whole genome gene expression survey
2007-12-01 | GSE7431 | GEO
Project description:We compared gene expression profiles between testes from C57BL/6 and C57BL/6-background congenic mouse strain B6.MRLc1-(D1Mit202–D1Mit403) carrying the telomeric region of MRL-type Chr 1 (67.97–81.63 cM) at 10 days after a single scrotal heat stress of 43°C for 20 min.
2014-08-01 | GSE53139 | GEO
Project description:Background and Aims: In the interleukin-10-deficient (Il10-/-) mouse model of IBD, 10 quantitative trait loci (QTL) have been shown to be associated with colitis susceptibility by linkage analyses on experimental crosses of highly susceptible C3H/HeJBir (C3Bir)-Il10-/- and partially resistant C57BL/6J (B6)-Il10-/- mice. The strongest locus (C3Bir-derived cytokine deficiency-induced colitis susceptibility [Cdcs]1 on Chromosome [Chr] 3) controlled multiple colitogenic subphenotypes and contributed the vast majority to the phenotypic variance in cecum and colon. This was demonstrated by interval-specific Chr 3 congenic mice wherein defined regions of Cdcs1 from C3Bir or B6 were bred into the IL-10-deficient reciprocal background and altered the susceptible or resistant phenotype. Furthermore, this locus likely acts by inducing innate hypo- and adaptive hyperresponsiveness, associated with impaired NFΚB responses of macrophages. The aim of the present study was to dissect the complexity of Cdcs1 by further development and characterization of reciprocal Cdcs1 congenic strains and to identify potential candidate genes in the congenic interval. Material and Methods: In total, 15 reciprocal congenic strains were generated from Il10-/- mice of either C3H/HeJBir or C57BL/6J backgrounds by 10 cycles of backcrossing. Colitis activity was monitored by histological grading. Candidate genes were identified by fine mapping of congenic intervals, sequencing, microarray analysis and a high-throughput real-time RT-PCR approach using bone marrow-derived macrophages. Results: Within the originally identified Cdcs1-interval, three independent regions were detected that likely contain susceptibility-determining genetic factors (Cdcs1.1, Cdcs1.2, and Cdcs1.3). Combining results of candidate gene approaches revealed Fcgr1, Cnn3, Larp7, and Alpk1 as highly attractive candidate genes with polymorphisms in coding or regulatory regions and expression differences between susceptible and resistant mouse strains. Conclusions: Subcongenic analysis of the major susceptibility locus Cdcs1 on mouse chromosome 3 revealed a complex genetic structure. Candidate gene approaches revealed attractive genes within the identified regions with homologs that are located in human susceptibility regions for IBD.
2009-10-01 | GSE15318 | GEO
Project description:Background and Aims: In the interleukin-10-deficient (Il10-/-) mouse model of IBD, 10 quantitative trait loci (QTL) have been shown to be associated with colitis susceptibility by linkage analyses on experimental crosses of highly susceptible C3H/HeJBir (C3Bir)-Il10-/- and partially resistant C57BL/6J (B6)-Il10-/- mice. The strongest locus (C3Bir-derived cytokine deficiency-induced colitis susceptibility [Cdcs]1 on Chromosome [Chr] 3) controlled multiple colitogenic subphenotypes and contributed the vast majority to the phenotypic variance in cecum and colon. This was demonstrated by interval-specific Chr 3 congenic mice wherein defined regions of Cdcs1 from C3Bir or B6 were bred into the IL-10-deficient reciprocal background and altered the susceptible or resistant phenotype. Furthermore, this locus likely acts by inducing innate hypo- and adaptive hyperresponsiveness, associated with impaired NFΚB responses of macrophages. The aim of the present study was to dissect the complexity of Cdcs1 by further development and characterization of reciprocal Cdcs1 congenic strains and to identify potential candidate genes in the congenic interval. Material and Methods: In total, 15 reciprocal congenic strains were generated from Il10-/- mice of either C3H/HeJBir or C57BL/6J backgrounds by 10 cycles of backcrossing. Colitis activity was monitored by histological grading. Candidate genes were identified by fine mapping of congenic intervals, sequencing, microarray analysis and a high-throughput real-time RT-PCR approach using bone marrow-derived macrophages. Results: Within the originally identified Cdcs1-interval, three independent regions were detected that likely contain susceptibility-determining genetic factors (Cdcs1.1, Cdcs1.2, and Cdcs1.3). Combining results of candidate gene approaches revealed Fcgr1, Cnn3, Larp7, and Alpk1 as highly attractive candidate genes with polymorphisms in coding or regulatory regions and expression differences between susceptible and resistant mouse strains. Conclusions: Subcongenic analysis of the major susceptibility locus Cdcs1 on mouse chromosome 3 revealed a complex genetic structure. Candidate gene approaches revealed attractive genes within the identified regions with homologs that are located in human susceptibility regions for IBD. Experiment Overall Design: Bone marrow derived macrophages (BMDM) of colitis susceptible C3Bir-Il10-/- and colitis resistant B6-Il10-/- as well as the Il10-/- reciprocal congenic strains CB-R1 (C3Bir genetic background carrying a long congenic chromosome 3 element containing Cdcs1 from B6, rendering this formerly susceptible background resistant) and BC-R3 (B6 genetic background that carries the Cdcs1-region of C3Bir) were cultured and stimulated with flagellin or left unstimulated. BMDM were obtained from 3 male mice per genotype and cultured in polystyrene 6-well culture plates. Before RNA-isolation, 3 wells per plate were stimulated with Cbir1 flagellin (and subsequently pooled for RNA isolation), the other 3 wells left unstimulated (and also pooled). In total, these experiments were replicated three times in order to perform microarray analyses in triplicates.
2009-10-09 | E-GEOD-15318 | biostudies-arrayexpress
Project description:We analyzed the differentiation of the bipotential gonad into a testis or an ovary in 2 strains of mice - 129S1/SvImJ (129S1) and C57BL/6J (B6). Our results provide a high resolution view of the initiation and canalization of the differentiation of the gonad. It also reveals global differences in the transcriptome between 129S1 and B6 mice.
2013-06-11 | GSE41948 | GEO