Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA128565 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The signaling cascades that direct the morphological differentiation of the vascular system during early embryogenesis are not well defined. To further understand the role of Notch signaling during endothelial differentiation, this study uses both an in vivo gain-of-function and in vivo loss-of-function approach. At embryonic day 9.5, embryos with activated Notch1 signaling in the endothelia display a variety of growth and cardiovascular defects, and die soon after E10.5. Most notably, the extra-embryonic vasculature of the yolk sac displays remodeling differentiation defects. In the wild-type yolk sac, the primary vascular network has begun to reorganize, forming the large primary vessels and the smaller capillaries. In the activated Notch1 embryos remodeling is defective; the vasculature have an enlarged surface with decreased inter-vessel space. Embryos with ablated Notch signaling also display growth and vascular defects at E9.5 similar to the activated Notch1 embryos, however they exhibit a lack of vascular remodeling in the yolk sac, retaining the simple vascular plexus seen at E8.5. These results indicate that Notch signaling plays a critical role in the remodeling of the vasculature in the early embryo, particularly in the extra embryonic region. A conditional transgenic system was used in this study to activate Notch signaling. The ubiquitous ROSA26Notch transgene with a Neo/stop cassette flanked by loxP sites, followed by the N1-ICD cDNA, was recombined with a Tie2-CRE mouse, resulting in the removal of the STOP cassette and the subsequent activation of the Notch1-intracellular domain. This allowed for the overexpression and expansion of Notch signaling in all endothelial cells. Male Tie2-Cre mice were mated with female ROSA26Notch mice and resulting embryos were dissected at embryonic day 9.5. To ablate Notch signaling, Tie2-Cre mice were used in a two generation cross to obtain Tie2-Cre; Rbpj flox/flox embryos. These embryos lack RBPJ binding activity in the endothelia. In both instances embryos were used for genotyping and the yolk sac were separated and used to isolate total RNA with an RNeasy mini kit. The RNA was analyzed with the Mouse Genome 430A Array from Affymetrix. Samples were performed in duplicate, and RNA from wild type yolk sac tissues was compared to activated Notch and RBPJ loss-of-function yolk sac tissues.
2010-07-07 | E-GEOD-22418 | biostudies-arrayexpress
Project description:The signaling cascades that direct the morphological differentiation of the vascular system during early embryogenesis are not well defined. To further understand the role of Notch signaling during endothelial differentiation, this study uses both an in vivo gain-of-function and an in vivo loss-of-function approach. At embryonic day 9.5, embryos with activated Notch1 signaling in the endothelia display a variety of growth and cardiovascular defects, and die soon after E10.5. Most notably, the extra-embryonic vasculature of the yolk sac displays remodeling differentiation defects. In the wild-type yolk sac, the primary vascular network has begun to reorganize, forming the large primary vessels and the smaller capillaries. In the activated Notch1 embryos, remodeling is defective; the vasculature have an enlarged surface with decreased inter-vessel space. Embryos with ablated Notch signaling also display growth and vascular defects at E9.5 similar to the activated Notch1 embryos, however they exhibit a lack of vascular remodeling in the yolk sac, retaining the simple vascular plexus seen at E8.5. These results indicate that Notch signaling plays a critical role in the remodeling of the vasculature in the early embryo, particularly in the extra-embryonic region.
2010-06-18 | GSE22418 | GEO
Project description:GW182 (Tnrc6a) is a key component of RISC (miRNA-Induced Silencing Complex) that plays a critical role in miRNA-mediated gene silencing. Here, we show that GW182 is expressed in the yolk sac endoderm, and that gene-trap disruption of GW182 leads to growth arrest of yolk sac endoderm, impaired hematopoiesis and embryonic lethality. To investigate roles of GW182 in the yolk sac endoderm, we assessed changes in mRNA expression in the yolk sac of E9.5 GW182gt/gt embryos using microarrays (Affymetrix).
2011-09-01 | GSE30244 | GEO
Project description:GW182 (Tnrc6a) is a key component of RISC (miRNA-Induced Silencing Complex) that plays a critical role in miRNA-mediated gene silencing. Here, we show that GW182 is expressed in the yolk sac endoderm, and that gene-trap disruption of GW182 leads to growth arrest of yolk sac endoderm, impaired hematopoiesis and embryonic lethality. To investigate roles of GW182 in the yolk sac endoderm, we assessed changes in mRNA expression in the yolk sac of E9.5 GW182gt/gt embryos using microarrays (Affymetrix). Yolk sac of wild type littermates and GW182gt/gt embryos at E9.5 was collected for total RNA isolation using Trizol (Invitrogen). RNAs were purified according to the manufacturer’s protocol before subjected to Mouse Gene 1.0 ST Whole Genome Array (Affymetrix) for mRNA expression profiling. Experiments were performed in triplicate. Differentially expressed mRNAs were identified using a two-sample t-test (P<0.05 considered significant).
2011-08-31 | E-GEOD-30244 | biostudies-arrayexpress
Project description:Primitive erythropoiesis in the mouse yolk sac is followed by definitive erythropoiesis resulting in adult erythrocytes. In comparison to definitive erythropoiesis little is known about the genes that control the embryonic erythroid program. The purpose of this study was to generate a profile of mouse embryonic yolk sac erythroid cells and identify novel regulatory genes differentially expressed in erythroid compared to non-erythroid (epithelial cells). The identification of these genes will contribute to a greater understanding of how the primitive erythroid program is controlled. This work will have clinical implications for treating sickle cell anemia and β-thalassemia. Activating genes in adult erythroid cells that increase embryonic or fetal globin gene expression may be a therapeutic approach to treat individuals with these disorders. Experiment Overall Design: Embryonic day 9.5 (E9.5) yolk sacs were dissected from the embryos of timed-pregnant FVB/N mice. These tissues were frozen in OCT media and 8-micron frozen sections were obtained. Laser capture microdissection (LCM) was used to isolate primitive erythroid precursors and epithelial cells from these E9.5 yolk sac frozen sections using 2 to 4 yolk sacs from 2 different litters per biological replicate. Paired erythroid and epithelial samples were collected from the same microscope slides. Total RNA was isolated from 4 different pairs of erythroid and epithelial samples and hybridized to Affymetrix 430 A 2.0 microarrays.
2008-06-11 | E-GEOD-10002 | biostudies-arrayexpress
Project description:The yolk sac is a vital extraembryonic organ that supports embryonic development during early gestation, before the placenta assumes many of its supportive functions. Abnormal development or function of the yolk sac can lead to embryonic demise or developmental abnormalities. However, the genetic and environmental factors that impair human yolk sac development and function remain poorly understood. Human yolk sac models that are amenable to experimental manipulation would therefore be valuable for investigating these mechanisms. The long-term goal of this study is to establish an in vitro model of the human yolk sac from pluripotent stem cells. As an initial step toward this goal, we investigated whether three-dimensional aggregates of human embryonic stem cells could be induced toward a primitive endoderm-like state, which gives rise to the yolk sac during embryonic development.
2026-09-16 | GSE347287 | GEO
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:Primitive erythropoiesis in the mouse yolk sac is followed by definitive erythropoiesis resulting in adult erythrocytes. In comparison to definitive erythropoiesis little is known about the genes that control the embryonic erythroid program. The purpose of this study was to generate a profile of mouse embryonic yolk sac erythroid cells and identify novel regulatory genes differentially expressed in erythroid compared to non-erythroid (epithelial cells). The identification of these genes will contribute to a greater understanding of how the primitive erythroid program is controlled. This work will have clinical implications for treating sickle cell anemia and β-thalassemia. Activating genes in adult erythroid cells that increase embryonic or fetal globin gene expression may be a therapeutic approach to treat individuals with these disorders. Keywords: Comparison between mouse embryonic day 9.5 yolk sac microdissected primitive erythroid precursors and epithelial cells
2008-01-03 | GSE10002 | GEO
Project description:This study aimed at exploring the physiological function of mammalian HYPB by means of knockout mouse model. Homogenous disruption of mouse Hypb gene leads to embryonic lethality at E10.5-E11.5. Severe vascular defects were observed in the Hypb-/- embryos, yolk sac and placenta.In the mutant embryo and yolk sac, disorganized and abnormally dilated capillaries cannot be remodeled into large blood vessels or intricate networks. Thus, our results suggest that the mammalian HYPB HMT plays an important role in embryonic vascularization. Keywords: knockout, mouse embryo development, angiogenesis, yolk sac, E9.0, E10.5
2009-12-28 | GSE10113 | GEO
Project description:ESCO2 encodes a cohesin acetyltransferase required for embryonic development, but how ESCO2 deficiency disrupts endothelial cell state and vascular development remains incompletely understood. This study used conditional Esco2 deletion in embryonic yolk sac endothelium to investigate gene-expression, transcript-isoform, and chromatin-occupancy changes associated with endothelial dysfunction. Short-read single-cell RNA sequencing of E9.5 control and Esco2-deficient yolk sacs was used to define endothelial and endothelial-to-mesenchymal transition (EndMT)-associated cell states. Single-cell long-read isoform sequencing (ScISOr-seq) was used to resolve transcript isoform usage and identify isoform switching not apparent from gene-level expression. In parallel, Esco2 CUT&Tag was performed on FACS-isolated GFP+ Lyve1-lineage cells from E9.5 yolk sacs to define genomic regions associated with Esco2 occupancy. Together, these datasets provide complementary gene-level, isoform-level, and chromatin-occupancy profiles for investigating Esco2-dependent regulation of endothelial state during early vascular development.
2026-09-14 | GSE344313 | GEO