Disease relevance of Ysg1

• Most of the cells were similar to those found in so-called "parietal yolk sac carcinomas," secreted Reichert's membrane-like material, and could be found in subsequent transplant generations [1].
• These yolk sac cells could grow and give rise to malignant, transplantable tumors identical to mouse yolk sac carcinomas derived from teratocarcinoma [2].
• Visceral yolk sac sarcomas have not previously been reported; the MB4-derived tumor may prove to be the first [1].
• This report covered the pathologic features, behavior, metastases, and results of transplantation of pure yolk sac carcinomas that were primary in the uterine horn of 8 mice; 6 mice were strain C3H and 2 were strain HR, and they varied from 10 to 23 months of age [3].
• In contrast to the high numbers of receptor sites found in Ewing's sarcomas (55-640 fmol x mg-1 protein; dissociation constant Kd, 1-2 nM), other childhood cancers (neuroblastoma, rhabdomyosarcoma, brain tumors, lymphoma, osteosarcoma, hepatoblastoma, yolk sac, and Wilms' tumor) contained in general fewer beta-adrenergic receptor sites [4].

Psychiatry related information on Ysg1

• The deficiency of MHC antigens in the apical membrane may account for the failure of sensitized females to reject the yolk sac, whereas the composition of the laterobasal membrane is probably less important to maternal-fetal relations [5].
• TGFbeta inhibition of yolk-sac-like differentiation of human embryonic stem-cell-derived embryoid bodies illustrates differences between early mouse and human development [6].

High impact information on Ysg1

• HoxB4 confers definitive lymphoid-myeloid engraftment potential on embryonic stem cell and yolk sac hematopoietic progenitors [7].
• In an effort to characterize factors that distinguish the definitive adult hematopoietic stem cell (HSC) and primitive progenitors derived from yolk sac or embryonic stem (ES) cells, we examined the effect of ectopic expression of HoxB4, a homeotic selector gene implicated in self-renewal of definitive HSCs [7].
• Map3k3-/- embryos died at approximately embryonic day (E) 11, displaying disruption of blood vessel development and the structural integrity of the yolk sac [8].
• Embryos homozygous for the Hand1 null allele died between embryonic days 8.5 and 9.5 and exhibited yolk sac abnormalities due to a deficiency in extraembryonic mesoderm [9].
• We also demonstrate that cells lacking Flk1 are unable to reach the correct location to form blood islands, suggesting that Flk1 is involved in the movement of cells from the posterior primitive streak to the yolk sac and, possibly, to the intraembryonic sites of early hematopoiesis [10].

Chemical compound and disease context of Ysg1

• We used antibodies raised against both a heparan sulfate proteoglycan purified from a mouse sarcoma and a chondroitin sulfate proteoglycan purified from a rat yolk sac carcinoma to study the appearance and distribution of proteoglycans in cultured cells [11].
• Apolipoprotein E (apoE) expression was studied in F9 embryonal carcinoma cells that differentiate in response to retinoic acid into cells resembling either parietal endoderm or visceral endoderm of the parietal or visceral yolk sac [12].
• In this report we demonstrate that exposure to hyperglycemia during gastrulation causes yolk sac and embryonic vasculopathy in cultured murine conceptuses and in the conceptuses of streptozotocin-induced diabetic pregnant mice [13].
• SSEA-1, the antigen found on mouse embryonal carcinoma (EC) cells and embryonic cells from the 8-cell stage embryo onward, including the fetal primordial germ cells, was detected on yolk sac carcinoma components of human tumors, but not on EC cells [14].
• Coxiella burnetii, phase I and II, cells cultivated in the yolk sac of chicken embryos were separated from host cell components by two cycles of isopycnic Renografin gradient centrifugation [15].

Biological context of Ysg1

• Two sites of hematopoietic activity, the yolk sac and aorta-gonad-mesonephros (AGM) region, function in mouse ontogeny at the pre-liver stage of hematopoiesis [16].
• Phenotyping of mRNA demonstrated exclusive expression from the paternal allele in all embryonic tissues, including visceral yolk sac, between 11 and 12.5 days of gestation [17].
• Analysis indicated that embryonic erythropoiesis, which occurs in the yolk sac, was not impaired by the c-myb alteration [18].
• If it is correct that the visceral endoderm of the early embryo makes a major contribution to the formation of the endoderm portion of the visceral yolk sac, then it is clear that a switch in collagen gene expression must occur as it does so [19].
• Preferential expression of the maternally derived X chromosome in the mouse yolk sac [20].

Anatomical context of Ysg1

• Little or no type IV collagen synthesis was detected in the endoderm of the visceral yolk sac [19].
• The endoderm of the visceral yolk sac was shown to be synthesizing primarily type I collagen, while the mesoderm layer of this membrane synthesized both type I and IV collagens [19].
• The endodermal portion of the visceral yolk sac did not react, while small amounts were found in the amnion [19].
• Two types of tissues have been examined with respect to randomness of inactivation in 14-day mouse conceptuses: 1) fetal tissue, which undergoes random inactivation of either the maternal or paternal X; and 2) yolk sac endoderm tissue, an extraembryonic membrane, which normally undergoes nonrandom inactivation of the paternal X [21].
• It is widely accepted that during murine embryogenesis, totipotent haematopoietic stem cells first originate in the yolk sac, then migrate to the fetal liver and finally colonize the bone marrow shortly before birth [22].

Associations of Ysg1 with chemical compounds

• Administration of AGM-1470 to pregnant mice resulted in complete failure of embryonic growth due to interference with decidualization, placental and yolk sac formation, and embryonic vascular development [23].
• In addition, the 89-kd and 59-kd HSP are not stimulated by an arsenite shock in contrast to what is observed with fibroblasts or cells of the parietal yolk sac type [24].
• Presomitic and 3- to 12-somite pair cultured mouse embryos were deprived of retinoic acid (RA) by yolk-sac injections of antisense oligodeoxynucleotides for retinol binding protein (RBP) [25].
• Developmental abnormalities in cultured mouse embryos deprived of retinoic by inhibition of yolk-sac retinol binding protein synthesis [25].
• Embryos stain weakly with benzidine reagent, and yolk sac cells express globin RNAs, indicating globin gene activation in the absence of GATA-1 [26].

Physical interactions of Ysg1

• L-2-Oxothiazolidine-4-carboxylate (OTC), a cysteine prodrug, prevented oxidative stress and the induction of AP-1 binding activity in the embryo but not in the yolk sac [27].
• The physicochemical characteristics of cytosolic glucocorticoid-receptor complexes were examined by DEAE-Sephadex A-50 column chromatography. "Unactivated" complexes from visceral yolk sac, fetal and adult liver eluted at approx. 0.4 M KCl [28].

Regulatory relationships of Ysg1

• In mouse, Gatm is expressed during development and is imprinted in the placenta and yolk sac, but not in embryonic tissues [29].
• Thus, under certain growth factor conditions, Tpo directly inhibits early yolk sac erythroid CFU growth but facilitates megakaryocyte and mixed lineage colony formation [30].
• Flow-cytometric analysis showed that hemopoiesis in the yolk sac and fetal liver started from cells that express c-Kit [31].
• Fzd5 mRNA was expressed in the yolk sac, eye and lung bud at 9.5 days post coitum [32].
• In the developing embryo, Vezf1 is expressed in the yolk sac mesoderm and the endothelium of the developing vasculature and, in addition, in mesodermal and neuronal tissues [33].

Other interactions of Ysg1

• A modest decline in Ins-2 RNA was observed in the yolk sac [34].
• During early development of the mouse embryo, expression of the metallothionein-I (MT-I) gene is heightened specifically in the endoderm cells of the visceral yolk sac [35].
• PECAM staining of yolk sac endothelial cells showed the absence of branching arteries and veins, the absence of a capillary bed, and the presence of large avascular spaces between the blood vessels [36].
• Expression of Ipl is highest in placenta and yolk sac, where its mRNA is derived almost entirely from the maternal allele [37].
• Here, we show that deletion of the C-terminal half of Bruce, including the UBC domain, causes activation of caspases and apoptosis in the placenta and yolk sac, leading to embryonic lethality [38].

Analytical, diagnostic and therapeutic context of Ysg1

• We report the molecular cloning of two groups of genes expressed in the yolk sac: a group of genes expressed in the day-8.5 yolk sac at higher levels than in the day-8.5 embryo proper and up-regulated during EB development, and another group of day-8.5 yolk sac genes not expressed in the day-8.5 embryo proper or in EBs [39].
• We report here that approximately half of homozygous embryos deficient in factor V (Fv-/-), which have been generated by gene targeting, die at embryonic day (E) 9-10, possibly as a result of an abnormality in the yolk-sac vasculature [40].
• Here, we separated yolk sac and intraembryonic splanchnopleura prior to circulation and maintained the explants in organ culture before transfer [41].
• In addition, we show by in situ hybridization to tissue sections that all endoderm cells of the visceral yolk sac contain AFP mRNA, indicating that the visceral endoderm layer is a homogeneous population of cells with respect to transcription of the AFP gene [42].
• We show here that cell suspensions from day 7 early-mid-primitive streak stage embryo proper generated early immature PgP-1+ Joro 177+ Lin- hematopoietic cells and some Mac-1+ myeloid and TER 119+ erythroid cells after co-culture with the yolk sac-derived stromal cell line YS6 without addition of exogenous cytokines [43].

References