Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Parallel tracking dosage compensation in the early mouse embryo

ABSTRACT: We develop So-Smart-seq to interrogate a comprehensive transcriptome inclusive of coding, noncoding, and repetitive element transcription. We reveal that, surprisingly, de novo silencing pertains only to a subset of paternal X (Xp) genes. In contrast, a set of evolutionarily older genes and LINEs demonstrate constitutive Xp silencing, adopt epigenetically distinct signatures, and do not require Xist to initiate silencing. On maternal X (Xm), however, these elements are hyperactivated. Thus, a significant subset of Xp elements appears to be inherited in a “pre-inactive” state. We also find that Xm-hyperactivation is timed to Xp silencing on an individual gene basis, giving rise to heterogeneity in the parallel track of dosage compensation as well. These conclusions have significant implications for the mechanism and evolution of imprinting in early mammals.

ORGANISM(S): Mus musculus Mus musculus castaneus

PROVIDER: GSE168455 | GEO | 2024/03/15

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Sex chromsomes affect gene expression of immunized CD4+ T cells in SJL

Project description:To determine the role of sex chromsomes in sex differences of autoimmune disease, we used high throughput RNA sequencing to analyze the transciptomes of CD4+ T cells stimuated with anti-CD3/CD28 from XX and XY- mice using the “four core genotypes” mouse model. We found higher expression of several X genes in the XY- genotype compared to XX, suggesting a difference in DNA methylation of these genes between Xp and Xm. In a hypothesis driven targeted approach, we investigated two immunomodulatory X genes, Tlr7 and FoxP3 and found that the promoter regions of both genes had more DNA methylation on the Xp than Xm, and that both genes had higher expression in autoantigen stimulated CD4+ T cells from XY- compared to XX mice. This study provides new insights regarding how sex chromsomes affect gene expression and cause sex differences in autoimmune disease.

2019-12-10 | GSE139035 | GEO

Sex chromsomes affect gene expression of healthy CD4+ T cells in B6 gonadal males

Project description:To determine the role of sex chromsomes in sex differences of autoimmune disease, we used high throughput RNA sequencing to analyze the transciptomes of CD4+ T cells stimuated with antiCD3/CD28 from XXSry and XY-Sry mice using the “four core genotypes” mouse model. We found higher expression of several X genes in the XY- genotype compared to XX, suggesting a difference in DNA methylation of these genes between Xp and Xm. In a hypothesis driven targeted approach, we investigated two immunomodulatory X genes, Tlr7 and FoxP3 and found that the promoter regions of both genes had more DNA methylation on the Xp than Xm, and that both genes had higher expression in autoantigen stimulated CD4+ T cells from XY- compared to XX mice. This study provides new insights regarding how sex chromsomes affect gene expression and cause sex differences in autoimmune disease.

2019-12-10 | GSE139034 | GEO

Sex chromosomes affect gene expression of autoantigen specific CD4+ T cells in B6 gonadal males.

Project description:To determine the role of sex chromsomes in sex differences of autoimmune disease, we used high throughput RNA sequencing to analyze the transciptomes of autoantigen specific CD4+ T cells from XX and XY- mice using the “four core genotypes” mouse model. We found higher expression of several X genes in the XY- genotype compared to XX, suggesting a difference in DNA methylation of these genes between Xp and Xm. In a hypothesis driven targeted approach, we investigated two immunomodulatory X genes, Tlr7 and FoxP3 and found that the promoter regions of both genes had more DNA methylation on the Xp than Xm, and that both genes had higher expression in autoantigen stimulated CD4+ T cells from XY- compared to XX mice. This study provides new insights regarding how sex chromsomes affect gene expression and cause sex differences in autoimmune disease.

2019-12-10 | GSE137793 | GEO

Sex chromosomes affect gene expression of healthy CD4+ T cells in SJL.

2019-12-10 | GSE137792 | GEO

Sex chromosomes affect gene expression of healthy CD4+ T cells in B6 gonadal females.

Project description:To determine the role of sex chromsomes in sex differences of autoimmune disease, we used high throughput RNA sequencing to analyze the transciptomes of CD4+ T cells stimuated with antiCD3/CD28 from XX and XY- mice using the “four core genotypes” mouse model. We found higher expression of several X genes in the XY- genotype compared to XX, suggesting a difference in DNA methylation of these genes between Xp and Xm. In a hypothesis driven targeted approach, we investigated two immunomodulatory X genes, Tlr7 and FoxP3 and found that the promoter regions of both genes had more DNA methylation on the Xp than Xm, and that both genes had higher expression in autoantigen stimulated CD4+ T cells from XY- compared to XX mice. This study provides new insights regarding how sex chromsomes affect gene expression and cause sex differences in autoimmune disease.

2019-12-10 | GSE137791 | GEO

Transcription profiling of mouse whole brain gene expression in X-monosomic and normal female mice

Project description:Whole brain gene expression was examined in the following strains of mice: 1. P0 maternal monosomic 39,Xm females, C57BL/6J x C3H/Paf; 2. P0 paternal monosomic 39, Xp females, In(X)/C3H x C57BL/6J; 3. P0 normal 40,XX females, In(X)/C3H x C57BL/6J; 4. P0 normal 40,XX females, C57BL/6J x C3H/Paf

2007-10-11 | E-GEOD-1606 | biostudies-arrayexpress

Whole brain gene expression in X-monosomic and normal female mice

Project description:Whole brain gene expression was examined in the following strains of mice: 1. P0 maternal monosomic 39,Xm females, C57BL/6J x C3H/Paf 2. P0 paternal monosomic 39, Xp females, In(X)/C3H x C57BL/6J 3. P0 normal 40,XX females, In(X)/C3H x C57BL/6J 4. P0 normal 40,XX females, C57BL/6J x C3H/Paf Keywords = imprinting Keywords = mammalian genetics Keywords = X-linked Keywords = brain Keywords: other

2005-05-02 | GSE1606 | GEO

Intragraft Gene Expression in Positive Crossmatch Kidney Allografts: Ongoing Inflammation Mediates Chronic Antibody-Mediated Injury

Project description:We studied intragraft gene expression profiles of positive crossmatch (+XM) kidney transplant recipients who develop transplant glomerulopathy (TG) and those who do not. Whole genome microarray analysis and quantitative rt-PCR for 30 transcripts were performed on RNA from protocol renal allograft biopsies in 3 groups: 1) +XM/TG+ biopsies before and after TG; 2) +XM/NoTG; and 3) negative crossmatch kidney transplants (control). Microarray comparisons showed few differentially expressed genes between paired biopsies from +XM/TG+ recipients before and after the diagnosis of TG. Comparing +XM/TG+ and control groups, significantly altered expression was seen for 2,447 genes (18%) and 3,200 genes (24%) at early and late time points, respectively. Canonical pathway analyses of differentially expressed genes showed inflammatory genes associated with innate and adaptive immune responses. Comparing +XM/TG+ and +XM/NoTG groups, 3,718 probe sets were differentially expressed but these were over-represented in only 4 pathways. A classic accommodation phenotype was not identified. Using rt-PCR, the expression of inflammatory genes was significantly increased in +XM/TG+ recipients compared to control biopsies and to +XM/NoTG biopsies. In conclusion, pre-transplant DSA results in a gene expression profile characterized by inflammation and cellular infiltration and the majority of XM+ grafts are exposed to chronic injury.

2012-05-30 | GSE34748 | GEO

Insights from multi-omic modelling of neurodegeneration in Xeroderma Pigmentosum using an induced pluripotent stem cell system

Project description:Xeroderma pigmentosum (XP) is caused by defective nucleotide excision-repair of DNA damage. This results in hypersensitivity to ultraviolet light and increased skin cancer risk, as sunlight-induced photoproducts remain unrepaired. However, many XP patients also display early-onset neurodegeneration, which leads to premature death. The mechanism of neurodegeneration is unknown. Here, we investigate XP neurodegeneration using pluripotent stem cells derived from XP patients and healthy relatives, performing functional multi-omics on samples during neuronal differentiation. We show substantially increased levels of 5',8-cyclopurine and 8-oxopurine in XP neuronal DNA secondary to marked oxidative stress. Furthermore, we find that the endoplasmic reticulum stress response is upregulated and reversal of the mutant genotype is associated with phenotypic rescue. Critically, XP neurons exhibit inappropriate downregulation of the protein clearance ubiquitin-proteasome system (UPS). Chemical enhancement of UPS activity in XP neuronal models improves phenotypes, albeit inadequately. Although more work is required, this study presents insights with intervention potential.

2024-04-18 | PXD047571 | Pride

Intragraft Gene Expression in Positive Crossmatch Kidney Allografts: Ongoing Inflammation Mediates Chronic Antibody-Mediated Injury

2012-05-30 | E-GEOD-34748 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data