Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA107627 | ENA |
REPOSITORIES: ENA
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Project description:The reduced folate carrier (RFC1) is an integral membrane protein and facilitative anion exchanger that mediates delivery of 5-methyltetrahydrofolate into mammalian cells. Adequate maternal-fetal transport of folate is necessary for normal embryogenesis. Targeted inactivation of the murine RFC1 gene results in post-implantation embryo lethality, but daily folic acid supplementation of pregnant dams prolongs survival of homozygous embryos until mid-gestation. At E10.5 RFC1-/- embryos are developmentally delayed relative to wildtype littermates, have multiple malformations, including neural tube defects, and die due to failure of chorioallantoic fusion. The mesoderm is sparse and disorganized, and there is a marked absence of erythrocytes in yolk sac blood islands. Affymetrix microarray analysis and quantitative RT-PCR validation of the relative gene expression profiles in E9.5 RFC1-/- vs. RFC1+/+ embryos indicates a dramatic downregulation of multiple genes involved in erythropoiesis, and upregulation of several genes that form the cubilin-megalin multiligand endocytic receptor complex. Megalin protein expression disappears from the visceral yolk sac of RFC1-/- embryos, and cubilin protein is widely misexpressed. Inactivation of RFC1 impacts the expression of several ligands and interacting proteins in the cubilin-amnionless-megalin complex that are involved in the maternal-fetal transport of folate, vitamin B12, and other nutrients, lipids and morphogens required for normal embryogenesis. Comparison of RFC KO, wildtype normal embryos vs. RFC KO, nullizygous affected embryos Experiment Overall Design: 6 samples RFC KO mouse embryos, E9.5, folic acid treated: 3 Control, Wildtype, normal; 3 Affected, Nullizygous, CR/chorioallantoic defect; as paired-littermates with one normal and one affected embryo per set from each of three separate litters for RNA extraction and hybridization on Affymetrix microarrays.
2008-04-05 | E-GEOD-10659 | biostudies-arrayexpress
Project description:The reduced folate carrier (RFC1) is an integral membrane protein and facilitative anion exchanger that mediates delivery of 5-methyltetrahydrofolate into mammalian cells. Adequate maternal-fetal transport of folate is necessary for normal embryogenesis. Targeted inactivation of the murine RFC1 gene results in post-implantation embryo lethality, but daily folic acid supplementation of pregnant dams prolongs survival of homozygous embryos until mid-gestation. At E10.5 RFC1-/- embryos are developmentally delayed relative to wildtype littermates, have multiple malformations, including neural tube defects, and die due to failure of chorioallantoic fusion. The mesoderm is sparse and disorganized, and there is a marked absence of erythrocytes in yolk sac blood islands. Affymetrix microarray analysis and quantitative RT-PCR validation of the relative gene expression profiles in E9.5 RFC1-/- vs. RFC1+/+ embryos indicates a dramatic downregulation of multiple genes involved in erythropoiesis, and upregulation of several genes that form the cubilin-megalin multiligand endocytic receptor complex. Megalin protein expression disappears from the visceral yolk sac of RFC1-/- embryos, and cubilin protein is widely misexpressed. Inactivation of RFC1 impacts the expression of several ligands and interacting proteins in the cubilin-amnionless-megalin complex that are involved in the maternal-fetal transport of folate, vitamin B12, and other nutrients, lipids and morphogens required for normal embryogenesis. Comparison of RFC KO, wildtype normal embryos vs. RFC KO, nullizygous affected embryos Keywords: reduced folate carrier knockout, folate receptor, cubilin, megalin, embryos, gene expression, neural tube defect, chorioallantoic fusion
2008-03-17 | GSE10659 | GEO
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Project description:Comparison of conserved TAD boundaries reveals that diverging CTCF sites is an evolutionary conserved signature associated with TAD borders 4C-seq samples for six gene family promoters in different samples: E9.5 and E14.5 mouse embryos ; 24hpf, 48hpf, 80%epiboly and Dome zebrafish embryos ; 48hpf S.purpuratus embryos
2015-05-18 | E-GEOD-66900 | biostudies-arrayexpress
Project description:During embryonic development in mice, global deficiency of Trim71 (Trim71-KO) leads to defects in vascular development of the yolk sac and impaired primitive erythropoiesis. These phenotypes start to become apparent at E9.5. We analyzed changes in gene expression by single-cell RNA-sequencing (scRNA-seq) in whole Trim71-KO embryos compared to wildtype embryos at an early developmental stage (E7.5, late gastrulation) to investigate the onset of these phenotypes. Furthermore, we analyzed Trim71-KO and wildtype yolk sacs at E9.5 by scRNA-seq to gain insight into the changes in gene expression at the developmental stage when vascular defects have become apparent.
2025-02-04 | GSE272044 | GEO
Project description:Transcriptome changes in Slc7a5-null mouse embryos
2019-01-16 | E-MTAB-6336 | ExpressionAtlas
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Project description:Transcriptomic analysis of E9.5 mouse embryos
| PRJNA727827 | ENA
Project description:Transcriptional profiling of E9.5 mouse embryo tissue from the presomitic mesoderm (PSM) and somites I-IV. Tissue from embryos lacking a functional Paraxis gene (Paraxis-/-) was compared to identical tissue from E9.5 Wild Type embryos. The goal was to identify genes that had become deregulated in the absence of the transcription factor, Paraxis.
2013-12-05 | GSE47905 | GEO