Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA272746 | ENA |
REPOSITORIES: ENA
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Project description:Lymph node CD4+ T cell expression data from naïve C57BL/6J and C57BL/6J-ChrY^SJL
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Project description:The prevalence of some autoimmune diseases (AID) is greater in females compared with males, notwithstanding that disease severity is often greater in males. The reason for this sexual dimorphism (SD) is unknown, but may reflect negative selection of Y chromosome (ChrY) bearing sperm during spermatogenesis or male fetuses early in the course of conception/pregnancy. Previously, we showed that the SD in experimental autoimmune encephalomyelitis (EAE) is associated with copy number variation (CNV) in ChrY multicopy genes. Here, we test the hypothesis that CNV in ChrY multicopy genes influences the paternal parent-of-origin effect on EAE susceptibility in female mice. We show that C57BL/6J consomic strains of mice possessing an identical ChrX and CNV in ChrY multicopy genes exhibit a female biased sex-ratio and sperm head abnormalities, consistent with X-Y intragenomic conflict arising from an imbalance in CNV between homologous ChrX:ChrY multicopy genes. These males also display paternal transmission of EAE to female offspring and differential loading of miRNAs within the sperm nucleus. These findings provide evidence for a genetic mechanism at the level of the male gamete that contributes to the SD in EAE and paternal parent-of-origin effects in female mice, raising the possibility that a similar mechanism may contribute to the SD in MS. Three biological replicates for each strain were pooled from the axillary, brachial, and inguinal lymph nodes from 5 mice for each replicate. RNA was isolated from CD4+TCRB+ FAC sorted cells.
2015-01-16 | E-GEOD-65038 | biostudies-arrayexpress
Project description:Understanding the DNA elements that constitute and control the regulatory genome is critical for the appropriate therapeutic management of complex diseases. Here, using chromosome Y (ChrY) consomic mouse strains on the C57BL/6J background, we show that susceptibility to two diverse animal models of autoimmune disease, including experimental allergic encephalomyelitis (EAE) and experimental myocarditis, correlates with the natural variation in copy number of Sly and Rbmy multicopy ChrY genes. In the B6 background, ChrY possesses gene regulatory properties that impact both genome-wide gene expression and the presence of alternative splice variants in pathogenic CD4+ T cells. Using a ChrY consomic strain on the SJL background, we discovered a preference for ChrY-mediated gene regulation in macrophages, the immune cell subset underlying the EAE sexual dimorphism in SJL mice, rather than CD4+ T cells. Importantly, in both genetic backgrounds, an inverse correlation exists between the number of Sly and Rbmy ChrY gene copies and the number of significantly upregulated genes in immune cells, thereby supporting a link between copy number variation of Sly and Rbmy with the ChrY genetic element exerting regulatory properties. Moreover, in humans, an analysis of the CD4+ T cell transcriptome from male multiple sclerosis patients versus healthy controls provides further evidence for an evolutionarily conserved mechanism of gene regulation by ChrY. Thus, these data establish ChrY as a member of the regulatory genome in mammals due to its ability to regulate gene expression and alternative splicing in immune cells linked to disease.
2013-05-28 | GSE47437 | GEO
Project description:Understanding the DNA elements that constitute and control the regulatory genome is critical for the appropriate therapeutic management of complex diseases. Here, using chromosome Y (ChrY) consomic mouse strains on the C57BL/6J background, we show that susceptibility to two diverse animal models of autoimmune disease, including experimental allergic encephalomyelitis (EAE) and experimental myocarditis, correlates with the natural variation in copy number of Sly and Rbmy multicopy ChrY genes. In the B6 background, ChrY possesses gene regulatory properties that impact both genome-wide gene expression and the presence of alternative splice variants in pathogenic CD4+ T cells. Using a ChrY consomic strain on the SJL background, we discovered a preference for ChrY-mediated gene regulation in macrophages, the immune cell subset underlying the EAE sexual dimorphism in SJL mice, rather than CD4+ T cells. Importantly, in both genetic backgrounds, an inverse correlation exists between the number of Sly and Rbmy ChrY gene copies and the number of significantly upregulated genes in immune cells, thereby supporting a link between copy number variation of Sly and Rbmy with the ChrY genetic element exerting regulatory properties. Moreover, in humans, an analysis of the CD4+ T cell transcriptome from male multiple sclerosis patients versus healthy controls provides further evidence for an evolutionarily conserved mechanism of gene regulation by ChrY. Thus, these data establish ChrY as a member of the regulatory genome in mammals due to its ability to regulate gene expression and alternative splicing in immune cells linked to disease. Three biological replicates from young (M-bM-^IM-$4 weeks) and old (M-bM-^IM-% 6 months) mice from each strain were pooled from 5 mice for each replicate. RNA was isolated from CD4+TCRB+ FAC sorted cells and from thioglycollate-elicited peritoneal macrophages.
2013-05-28 | E-GEOD-47437 | biostudies-arrayexpress
Project description:Understanding the DNA elements that constitute and control the regulatory genome is critical for the appropriate therapeutic management of complex diseases. Here, using chromosome Y (ChrY) consomic mouse strains on the C57BL/6J background, we show that susceptibility to two diverse animal models of autoimmune disease, including experimental allergic encephalomyelitis (EAE) and experimental myocarditis, correlates with the natural variation in copy number of Sly and Rbmy multicopy ChrY genes. In the B6 background, ChrY possesses gene regulatory properties that impact both genome-wide gene expression and the presence of alternative splice variants in pathogenic CD4+ T cells compared to CD4+ T cells. An inverse correlation exists between the number of Sly and Rbmy ChrY gene copies and the number of significantly upregulated genes in immune cells, thereby supporting a link between copy number variation of Sly and Rbmy and the ChrY genetic element exerting regulatory properties. Thus, these data establish ChrY as a member of the regulatory genome in mammals due to its ability to regulate gene expression and alternative splicing in immune cells linked to disease. Three biological replicates for each strain were pooled from the axillary, brachial, and inguinal lymph nodes from 5 mice for each replicate. RNA was isolated from CD4+TCRB+ FAC sorted cells.
2013-05-17 | E-GEOD-47024 | biostudies-arrayexpress
Project description:Lymph node CD4+ T cell and thioglycollate-elicited peritoneal macrophage expression data from naïve young and old SJL/J and SJL-ChrY^B10.S male mice
| PRJNA205565 | ENA
Project description:Understanding the DNA elements that constitute and control the regulatory genome is critical for the appropriate therapeutic management of complex diseases. Here, using chromosome Y (ChrY) consomic mouse strains on the C57BL/6J background, we show that susceptibility to two diverse animal models of autoimmune disease, including experimental allergic encephalomyelitis (EAE) and experimental myocarditis, correlates with the natural variation in copy number of Sly and Rbmy multicopy ChrY genes. In the B6 background, ChrY possesses gene regulatory properties that impact both genome-wide gene expression and the presence of alternative splice variants, but not miRNA expression in pathogenic CD4+ T cells. An inverse correlation exists between the number of Sly and Rbmy ChrY gene copies and the number of significantly upregulated genes in immune cells, thereby supporting a link between copy number variation of Sly and Rbmy and the ChrY genetic element exerting regulatory properties. Thus, these data establish ChrY as a member of the regulatory genome in mammals due to its ability to regulate gene expression and alternative splicing in immune cells linked to disease. Three biological replicates for each strain were pooled from the axillary, brachial, and inguinal lymph nodes from 5 mice for each replicate. RNA was isolated from CD4+TCRB+ FAC sorted cells.
2013-05-28 | E-GEOD-47439 | biostudies-arrayexpress
Project description:The prevalence of some autoimmune diseases (AID) is greater in females compared with males, notwithstanding that disease severity is often greater in males. The reason for this sexual dimorphism (SD) is unknown, but may reflect negative selection of Y chromosome (ChrY) bearing sperm during spermatogenesis or male fetuses early in the course of conception/pregnancy. Previously, we showed that the SD in experimental autoimmune encephalomyelitis (EAE) is associated with copy number variation (CNV) in ChrY multicopy genes. Here, we test the hypothesis that CNV in ChrY multicopy genes influences the paternal parent-of-origin effect on EAE susceptibility in female mice. We show that C57BL/6J consomic strains of mice possessing an identical ChrX and CNV in ChrY multicopy genes exhibit a female biased sex-ratio and sperm head abnormalities, consistent with X-Y intragenomic conflict arising from an imbalance in CNV between homologous ChrX:ChrY multicopy genes. These males also display paternal transmission of EAE to female offspring and differential loading of miRNAs within the sperm nucleus. These findings provide evidence for a genetic mechanism at the level of the male gamete that contributes to the SD in EAE and paternal parent-of-origin effects in female mice, raising the possibility that a similar mechanism may contribute to the SD in MS.
2015-01-16 | GSE65047 | GEO