Origin and differentiation of the yolk sac and extraembryonic mesoderm in presomite human and rhesus monkey embryos

1978 ◽  
Vol 152 (1) ◽  
pp. 59-97 ◽  
Author(s):  
W. Patrick Luckett
Keyword(s):  
Rhesus Monkey ◽  
Yolk Sac ◽  
Extraembryonic Mesoderm

scholarly journals Initiation of hematopoiesis and vasculogenesis in murine yolk sac explants

Blood ◽  
1995 ◽  
Vol 86 (1) ◽  
pp. 156-163 ◽  
Author(s):  
J Palis ◽  
KE McGrath ◽  
PD Kingsley
Keyword(s):  
Endothelial Cells ◽  
Network Formation ◽  
Globin Gene ◽  
Primitive Streak ◽  
Yolk Sac ◽  
Vascular Network ◽  
Globin Mrna ◽  
Capillary Networks ◽  
Stage Of Development ◽  
Extraembryonic Mesoderm

The blood islands of the visceral yolk sac (VYS) are the initial sites of hematopoiesis in mammals. We have developed a yolk sac explant culture system to study the process of blood cell and endothelial cell development from extraembryonic mesoderm cells. No benzidine-positive cells or beta H1-globin mRNA expression was detected at the primitive streak or neural plate stage of development (E7.5). However, when isolated E7.5 dissected tissues were cultured for 36 to 72 hours in serum-free medium, hundreds of hemoglobin-producing cells and embryonic globin gene expression were identified in both intact yolk sac and VYS mesoderm explants. Explanted E7.5 extraembryonic mesoderm tissues thus recapitulate in vivo primitive erythropoiesis and do not require the presence of a vascular network or the VYS endoderm. Yolk sac blood islands also contain endothelial cells that arise by vasculogenesis and express flk-1. We detected flk-1 mRNA as early as the primitive streak stage of mouse embryogenesis. Culture of embryo proper and intact VYS explants, which contain both mesoderm and endoderm cells, produced capillary networks and expressed flk-1. In contrast, vascular networks were not seen when VYS mesoderm was cultured alone, although flk-1 expression was similar to that of intact VYS explants. The addition of vascular endothelial growth factor to VYS mesoderm explants did not induce vascular network formation. These results suggest that the VYS endoderm or its extracellular matrix is necessary for the coalescence of developing endothelial cells into capillary networks.

The orderly allocation of mesodermal cells to the extraembryonic structures and the anteroposterior axis during gastrulation of the mouse embryo

Development ◽  
1999 ◽  
Vol 126 (21) ◽  
pp. 4691-4701 ◽  
Author(s):  
S.J. Kinder ◽  
T.E. Tsang ◽  
G.A. Quinlan ◽  
A.K. Hadjantonakis ◽  
A. Nagy ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Mouse Embryo ◽  
Primitive Streak ◽  
Yolk Sac ◽  
Cell Lineages ◽  
Anteroposterior Axis ◽  
Extraembryonic Mesoderm ◽  
Extraembryonic Membranes ◽  
Lateral Mesoderm ◽  
Late Stages

The prospective fate of cells in the primitive streak was examined at early, mid and late stages of mouse gastrula development to determine the order of allocation of primitive streak cells to the mesoderm of the extraembryonic membranes and to the fetal tissues. At the early-streak stage, primitive streak cells contribute predominantly to tissues of the extraembryonic mesoderm as previously found. However, a surprising observation is that the erythropoietic precursors of the yolk sac emerge earlier than the bulk of the vitelline endothelium, which is formed continuously throughout gastrula development. This may suggest that the erythropoietic and the endothelial cell lineages may arise independently of one another. Furthermore, the extraembryonic mesoderm that is localized to the anterior and chorionic side of the yolk sac is recruited ahead of that destined for the posterior and amnionic side. For the mesodermal derivatives in the embryo, those destined for the rostral structures such as heart and forebrain mesoderm ingress through the primitive streak early during a narrow window of development. They are then followed by those for the rest of the cranial mesoderm and lastly the paraxial and lateral mesoderm of the trunk. Results of this study, which represent snapshots of the types of precursor cells in the primitive streak, have provided a better delineation of the timing of allocation of the various mesodermal lineages to specific compartments in the extraembryonic membranes and different locations in the embryonic anteroposterior axis.

scholarly journals Deficiency of Zonula Occludens-1 Causes Embryonic Lethal Phenotype Associated with Defected Yolk Sac Angiogenesis and Apoptosis of Embryonic Cells

2008 ◽  
Vol 19 (6) ◽  
pp. 2465-2475 ◽  
Author(s):  
Tatsuya Katsuno ◽  
Kazuaki Umeda ◽  
Takeshi Matsui ◽  
Masaki Hata ◽  
Atsushi Tamura ◽  
...  
Keyword(s):  
Yolk Sac ◽  
Embryonic Cells ◽  
Tissue Organization ◽  
Zonula Occludens ◽  
Cell Remodeling ◽  
Extraembryonic Mesoderm ◽  
Almost All ◽  
Vascular Trees ◽  
Induced Defects

Zonula occludens (ZO)-1/2/3 are the members of the TJ-MAGUK family of membrane-associated guanylate kinases associated with tight junctions. To investigate the role of ZO-1 (encoded by Tjp1) in vivo, ZO-1 knockout (Tjp1−/−) mice were generated by gene targeting. Although heterozygous mice showed normal development and fertility, delayed growth and development were evident from E8.5 onward in Tjp1−/− embryos, and no viable Tjp1−/− embryos were observed beyond E11.5. Tjp1−/− embryos exhibited massive apoptosis in the notochord, neural tube area, and allantois at embryonic day (E)9.5. In the yolk sac, the ZO-1 deficiency induced defects in vascular development, with impaired formation of vascular trees, along with defective chorioallantoic fusion. Immunostaining of wild-type embryos at E8.5 for ZO-1/2/3 revealed that ZO-1/2 were expressed in almost all embryonic cells, showing tight junction-localizing patterns, with or without ZO-3, which was confined to the epithelial cells. ZO-1 deficiency depleted ZO-1-expression without influence on ZO-2/3 expression. In Tjp1+/+ yolk sac extraembryonic mesoderm, ZO-1 was dominant without ZO-2/3 expression. Thus, ZO-1 deficiency resulted in mesoderms with no ZO-1/2/3, associated with mislocalization of endothelial junctional adhesion molecules. As a result, angiogenesis was defected in Tjp1−/− yolk sac, although differentiation of endothelial cells seemed to be normal. In conclusion, ZO-1 may be functionally important for cell remodeling and tissue organization in both the embryonic and extraembryonic regions, thus playing an essential role in embryonic development.

Differentiation of the embryonic disc, amnion, and yolk sac in the rhesus monkey

1986 ◽  
Vol 177 (2) ◽  
pp. 161-185 ◽  
Author(s):  
Allen C. Enders ◽  
Sandra Schlafke ◽  
Andrew G. Hendrickx
Keyword(s):  
Rhesus Monkey ◽  
Yolk Sac ◽  
Embryonic Disc

Transforming growth factor-beta signalling in extraembryonic mesoderm is required for yolk sac vasculogenesis in mice

Development ◽  
1999 ◽  
Vol 126 (16) ◽  
pp. 3473-3483
Author(s):  
M.J. Goumans ◽  
A. Zwijsen ◽  
M.A. van Rooijen ◽  
D. Huylebroeck ◽  
B.A. Roelen ◽  
...  
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Es Cells ◽  
Yolk Sac ◽  
Embryoid Bodies ◽  
Tgf Beta ◽  
Haematopoietic Cells ◽  
Growth Factor Beta ◽  
Extraembryonic Mesoderm

We have analysed the function of transforming growth factor beta (TGF-beta) in yolk sac development in mice by generating somatic chimaeras in which the extraembryonic mesoderm, which gives rise to the endothelial and haematopoietic cells of the yolk sac vasculature, is derived from embryonic stem (ES) cells. The ES cells were stably transfected and express either the full-length type II binding receptor or a kinase-deficient mutant of this receptor. Examination of yolk sacs from chimaeras between E8.5 and 9.5, and analysis of marker expression in embryoid bodies from these mutant ES cell lines in prolonged suspension culture demonstrated that (1) a major function of TGF-beta in yolk sac mesoderm is to regulate production and deposition of fibronectin in the extracellular matrix that maintains yolk sac integrity, (2) TGF-beta signalling is not required for differentiation of extraembryonic mesoderm into endothelial cells but is necessary for their subsequent organisation into robust vessels, and (3) TGF-beta signalling must be tightly regulated for the differentiation of primitive haematopoietic cells to take place normally. Together, these results show that defective TGF-beta signalling in the extraembryonic mesoderm alone is sufficient to account for the extraembryonic phenotype reported previously in TGF-beta1(−/−) mice (Dickson, M. C., Martin, J. S., Cousins, F. M., Kulkarni, A. B., Karlsson, S. and Akhurst, R. J. (1995) Development 121, 1845–1854).

Tissue-specific requirements for the proprotein convertase furin/SPC1 during embryonic turning and heart looping

Development ◽  
2000 ◽  
Vol 127 (2) ◽  
pp. 245-254 ◽  
Author(s):  
D.B. Constam ◽  
E.J. Robertson
Keyword(s):  
Serine Proteases ◽  
Es Cells ◽  
Embryonic Stem ◽  
Axial Rotation ◽  
Yolk Sac ◽  
Definitive Endoderm ◽  
Visceral Endoderm ◽  
Wild Type ◽  
Extraembryonic Mesoderm ◽  
Tissue Abnormalities

Furin, the mammalian prototype of a family of serine proteases, is required for ventral closure and axial rotation, and formation of the yolk sac vasculature. Here we show additionally that left-sided expression of pitx2 and lefty-2 are also perturbed in Furin-deficient embryos. These tissue abnormalities are preceded by a marked delay in the expansion of the definitive endoderm during gastrulation. Using a chimera approach, we show that Furin activity is required in epiblast derivatives, including the primitive heart, gut and extraembryonic mesoderm, whereas it is nonessential in the visceral endoderm. Thus, chimeric embryos, derived by injecting wild-type embryonic stem (ES) cells into fur(−/−) blastocysts, develop normally until at least 9.5 d.p.c. In contrast, Furin-deficient chimeras developing in the context of wild-type visceral endoderm fail to undergo ventral closure, axial rotation and yolk sac vascularization. Fur(−/−) cells are recruited into all tissues examined, including the yolk sac vasculature and the midgut, even though these structures fail to form in fur mutants. The presence of wild-type cells in the gut strikingly correlates with the ability of chimeric embryos to undergo turning. Overall, we conclude that Furin activity is essential in both extraembryonic and precardiac mesoderm, and in definitive endoderm derivatives.

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